{"id":6210,"date":"2026-08-13T12:19:46","date_gmt":"2026-08-13T12:19:46","guid":{"rendered":"https:\/\/www.ahmetozyigit.com\/?page_id=6210"},"modified":"2026-08-17T20:57:19","modified_gmt":"2026-08-17T20:57:19","slug":"zayiflama-igneleri","status":"publish","type":"page","link":"https:\/\/www.ahmetozyigit.com\/en\/tedaviler\/kilo-verme\/zayiflama-igneleri\/","title":{"rendered":"Slimming Injections (Ozempic, Mounjaro)"},"content":{"rendered":"
\"\"<\/figure>\n\n\n\n

Slimming Injections (Ozempic, Mounjaro)<\/strong>\n<\/p>\n\n\n\n

\n Losing weight should not be seen as a goal in itself, but as a tool for a healthier life. It is a known fact that overweight people have higher cardiovascular risks and are more likely to have health problems such as type 2 diabetes and metabolic syndrome. In addition to improving our appearance while losing weight, being healthier in biological and physiological aspects is an important goal for us.\n<\/p>\n\n\n\n

\n If you do not have enough information about weight control and healthy nutrition, it is very important to get help from a nutritionist. In addition, if you think you have an eating disorder and that this eating disorder has a psychological\/psychiatric basis, you should definitely consider getting help from a psychologist or psychiatrist. If you have reservations about this or do not know how to proceed, please ask for help during your consultation with Dr. Ahmet \u00d6zyi\u011fit. \n<\/p>\n\n\n\n

Injections Used for Weight Loss Purposes<\/strong>\n<\/p>\n\n\n\n

1- Liraglutide (Saxenda\u00ae)<\/strong>\n<\/p>\n\n\n\n

\n Liraglutide is one of the first-generation GLP-1 receptor agonists used in the treatment of obesity. Initially used in lower doses to treat type 2 diabetes, it was later introduced as Saxenda\u00ae at a daily dose of 3 mg for the treatment of obesity.\n<\/p>\n\n\n\n

\n GLP-1 is actually one of the hormones that our body naturally secretes after meals. It affects the appetite and satiety centers in the brain, slows gastric emptying, and increases glucose-dependent insulin secretion from the pancreas. Liraglutide activates GLP-1 receptors, prolonging the effect of this natural signal. As a result, a person may feel full sooner, stay full longer between meals, and experience a decrease in total energy intake.\n<\/p>\n\n\n\n

\n One of the most important studies on liraglutide in weight loss is the SCALE study, which included 3,731 obese or overweight adults. In the study, all participants were given support regarding nutrition and physical activity, and in addition, one group was given 3 mg of liraglutide daily, while the other group was given a placebo. At the end of 56 weeks, those using liraglutide experienced an average weight loss of 8.4 kg, or approximately %8 of their initial body weight, while in the placebo group this rate was approximately %2.6 [1].\n<\/p>\n\n\n\n

\n Elbette ortalama rakamlar her hastan\u0131n ayn\u0131 miktarda kilo verece\u011fi anlam\u0131na gelmez. Ayn\u0131 \u00e7al\u0131\u015fmada liraglutide kullanan hastalar\u0131n %63.2’si v\u00fccut a\u011f\u0131rl\u0131\u011f\u0131n\u0131n en az %5’ini, %33.1’i %10’dan fazlas\u0131n\u0131 ve %14.4’\u00fc %15’ten fazlas\u0131n\u0131 kaybetmi\u015ftir [1]. Yani liraglutide’\u0131n ger\u00e7ek ve klinik olarak anlaml\u0131 bir kilo verme etkisi vard\u0131r, ancak hastalar aras\u0131ndaki yan\u0131t olduk\u00e7a de\u011fi\u015fkendir.\n<\/p>\n\n\n\n

\n One of the disadvantages of liraglutide is that it is administered as a subcutaneous injection every day. Treatment is usually started at a low dose and gradually increased to 3 mg daily to reduce gastrointestinal side effects.\n<\/p>\n\n\n\n

\n The most common side effects are related to the gastrointestinal system. Nausea, vomiting, diarrhea, constipation, indigestion, and abdominal discomfort may occur. These complaints usually appear at the beginning of treatment or during dose increases and decrease over time in many patients. However, since later-developed injections such as semaglutide (Ozempic, Wegovy) and tyrzepatide (Mounjaro, Zepbound) have a much lower range of side effects compared to liraglutide and are more successful in terms of weight loss, saxenda is no longer a popular weight loss device worldwide. \n<\/p>\n\n\n\n

\n Due to the need for daily injections, the significant gastrointestinal side effects in some patients, and the average weight loss remaining in the range of approximately 1 TP3T8, we currently do not prefer liraglutide treatment for weight control in our center. \n<\/p>\n\n\n\n

2- Semaglutide (Wegovy\u00ae \/ Ozempic\u00ae)<\/strong>\n<\/p>\n\n\n\n

\n Semaglutide is a molecule that can be considered the second generation in GLP-1 therapies after liraglutide, and it represents a significant turning point in obesity treatment. Like liraglutide, it acts as a GLP-1 receptor agonist, but thanks to changes in its molecular structure, it remains active in the body for a much longer period. The most practical consequence of this is that it can be administered only once a week, not daily like liraglutide.\n<\/p>\n\n\n\n

\n Semaglutide was first introduced for the treatment of type 2 diabetes under the name Ozempic\u00ae. Later, due to its significant effects on weight control, Wegovy\u00ae was developed for the treatment of obesity at a dose of 2.4 mg weekly. It's important to clarify a common misconception: Ozempic and Wegovy both contain the same active ingredient, semaglutide. The brand differences are solely related to licensing and commercial aspects. \n<\/p>\n\n\n\n

\n Semaglutide’\u0131n kilo verme \u00fczerindeki ba\u015far\u0131s\u0131n\u0131 en net g\u00f6steren \u00e7al\u0131\u015fmalardan biri STEP 1 \u00e7al\u0131\u015fmas\u0131d\u0131r. Diyabeti olmayan, obez veya fazla kilolu 1.961 yeti\u015fkinin dahil edildi\u011fi bu \u00e7al\u0131\u015fmada, beslenme ve fiziksel aktivite d\u00fczenlemesine ek olarak haftada bir 2.4 mg semaglutide kullanan ki\u015filer 68 hafta sonunda ba\u015flang\u0131\u00e7 v\u00fccut a\u011f\u0131rl\u0131klar\u0131n\u0131n ortalama %14.9’unu kaybetmi\u015ftir. Plasebo grubunda ise kilo kayb\u0131 yaln\u0131zca %2.4 olmu\u015ftur [2].\n<\/p>\n\n\n\n

\n Belki daha da dikkat \u00e7ekici olan, semaglutide kullanan ki\u015filerin %86.4’\u00fcn\u00fcn v\u00fccut a\u011f\u0131rl\u0131\u011f\u0131n\u0131n en az %5’ini, %69.1’inin en az %10’unu ve %50.5’inin en az %15’ini kaybetmi\u015f olmas\u0131d\u0131r [2]. Bu sonu\u00e7lar semaglutide ile birlikte ila\u00e7la obezite tedavisinde ula\u015f\u0131labilecek kilo kayb\u0131 beklentisini ciddi \u015fekilde de\u011fi\u015ftirmi\u015ftir.\n<\/p>\n\n\n\n

\n Semaglutide’\u0131n \u00f6nemli \u00f6zelliklerinden biri de bu etkinin birka\u00e7 ayl\u0131k k\u0131sa bir d\u00f6nemle s\u0131n\u0131rl\u0131 kalmad\u0131\u011f\u0131n\u0131n g\u00f6sterilmi\u015f olmas\u0131d\u0131r. STEP 5 \u00e7al\u0131\u015fmas\u0131nda tedavi iki y\u0131l boyunca devam ettirilmi\u015f ve 104. haftada ortalama kilo kayb\u0131 %15.2 olarak korunmu\u015ftur [3]. Bu bize tedavi devam etti\u011fi s\u00fcrece semaglutide’\u0131n kilo kontrol\u00fc \u00fczerindeki etkisinin uzun vadede s\u00fcrd\u00fcr\u00fclebilece\u011fini g\u00f6stermektedir.\n<\/p>\n\n\n\n

\n GLP-1 receptors are located in several brain regions that control appetite and energy intake. Semagglutinin affects these systems, reducing hunger, increasing satiety, and decreasing a person's desire to eat. As a result, instead of constantly forcing themselves to restrict calories, a person may naturally start eating less.\n<\/p>\n\n\n\n

\n A common expression among patients is: \u201cI don\u2019t constantly think about food anymore.\u201d This actually describes the drug\u2019s effect on central appetite control quite well. One of the main mechanisms of weight loss with semagglutide is the reduction in daily energy intake [2]. It also increases glucose-dependent insulin secretion, regulates glucagon secretion, and can slow gastric emptying, especially at the beginning of treatment. Therefore, it has significant effects on glucose metabolism in addition to weight loss.\n<\/p>\n\n\n\n

\n The most common side effects of semaglutide, as with other GLP-1 receptor agonists, are related to the gastrointestinal system. The most frequent are: nausea, vomiting, diarrhea, constipation, bloating, and abdominal discomfort. However, it is important to consider not only the frequency of side effects but also their severity and the sustainability of treatment. Although gastrointestinal side effects have been reported quite frequently in STEP studies, the vast majority of them have been mild or moderate and transient. They occur more frequently, especially in the first weeks of treatment and during dose escalation, and decrease in many patients as the body adapts to the drug [2,3].\n<\/p>\n\n\n\n

\n Therefore, in semagglutide treatment, it is important to increase the dose slowly and in a controlled manner. I do not believe that every patient necessarily needs to reach the maximum dose. Similarly, it is not necessary to apply a standard four-week dose escalation program to every patient. The goal is not to use the highest possible dose, but to find the right balance between efficacy and tolerability for the patient. \n<\/p>\n\n\n\n

\n Therefore, the gastrointestinal side effects of semaglutide should definitely not be ignored, but with proper dose titration and patient selection, they remain manageable in many patients. It is particularly noteworthy that its side effect profile is more benign compared to liraglutide (Saxenda).\n<\/p>\n\n\n\n

\n There is also a small but real increased risk of gallstones and gallbladder disease. Since rapid and significant weight loss itself facilitates gallstone formation, it's not possible to attribute this entire risk directly to the medication.\n<\/p>\n\n\n\n

\n One of the concerns raised about semaglutide since its early days has been the risk of pancreatitis. However, we now have a considerable amount of clinical data, and the results of randomized controlled trials do not show that semaglutide use significantly increases the risk of acute pancreatitis. In a large meta-analysis evaluating a total of 34,721 patients in 21 randomized trials, the risk of acute pancreatitis was not increased in those using semaglutide compared to placebo, and similar results were seen for both low and high doses of subcutaneous semaglutide [5]. Similarly, in the safety analysis of the large SELECT study, which followed 17,604 overweight or obese patients, no significant increase in the incidence of pancreatitis was found with semaglutide 2.4 mg compared to placebo [6].\n<\/p>\n\n\n\n

\n Therefore, based on current clinical data, it is not accurate to say that semaglutide significantly increases the risk of pancreatitis compared to the general population. Since pancreatitis is a rare but serious disease, symptoms such as severe and persistent abdominal pain should certainly be evaluated during treatment; however, this clinical assessment does not mean that semaglutide has been shown to cause pancreatitis.\n<\/p>\n\n\n\n

\n Recently, there have been quite sensational reports linking semaglutide and tyrzepatide to "blindness." It's important to frame this correctly. A rare optic nerve disorder called non-arteritic anterior ischemic optic neuropathy (NAION) has been reported in some patients using semaglutide, and some observational studies suggest that this risk may be slightly increased in individuals using semaglutide. However, these studies do not prove that the drug directly causes NAION, and the absolute risk is quite low based on current data.\n<\/p>\n\n\n\n

\n In addition, the early worsening of diabetic retinopathy, a completely different mechanism, has long been known. In individuals who have lived with very high blood sugar for years and already have diabetic retinopathy, a rapid and drastic reduction in HbA1c can cause a temporary worsening of retinal findings. This is not unique to semaglutide; it is a phenomenon associated with rapid glycemic correction and has been previously described with potent glucose-lowering therapies, including insulin. The retinopathy signal observed in the SUSTAIN-6 study with semaglutide was also largely concentrated in patients who initially had retinopathy and experienced a rapid decrease in HbA1c.\n<\/p>\n\n\n\n

\n Therefore, statements like "Ozempic causes blindness" used on social media are nothing more than clickbait news that lacks scientific basis. \n<\/p>\n\n\n\n

3- Tirzepatide (Mounjaro\u00ae \/ Zepbound\u00ae)<\/strong><\/p>\n\n\n\n

\n Tirzepatide is a molecule that represents the next generation in obesity treatment and takes the classic GLP-1 approach a step further. Semagglutide only GLP-1 receptor<\/strong> while aiming, in tirepathy both at the same time GLP-1 and GIP receptors<\/strong> It activates it. Therefore, in tyrzepatia, one dual GIP\/GLP-1 receptor agonist<\/strong> It is defined as follows.\n<\/p>\n\n\n\n

\n GIP, like GLP-1, is a naturally occurring incretin hormone secreted from the intestines after meals. It plays a role in regulating insulin secretion, fat tissue metabolism, and energy balance. Tirzepatide's ability to target two different incretin systems simultaneously has resulted in a powerful effect not only on glucose control but also on appetite and body weight.\n<\/p>\n\n\n\n

\n Tirzepatide was initially used for the treatment of type 2 diabetes. Mounjaro\u00ae<\/strong> It was introduced under that name. After its effectiveness in the treatment of obesity was demonstrated, the same active ingredient was used. Zepbound\u00ae<\/strong> It is licensed under this name for weight control. It is administered subcutaneously once a week, and the dose is started at a low level and gradually increased to minimize gastrointestinal side effects. \n<\/p>\n\n\n\n

\n The most important study showing the effect of Tirzepatide on weight loss. SURMOUNT-1<\/strong> This study involved 2,539 adults who were obese or overweight but did not have diabetes. In this study, 5 mg, 10 mg, and 15 mg doses of thizzpatite were compared to placebo. After 72 weeks, the mean weight loss was:\n<\/p>\n\n\n\n

5 mg ile yakla\u015f\u0131k %15,<\/strong>\n<\/p>\n\n\n\n

10 mg ile yakla\u015f\u0131k %19.5,<\/strong>\n<\/p>\n\n\n\n

15 mg ile yakla\u015f\u0131k %20.9<\/strong> It has been found as such. \n<\/p>\n\n\n\n

\n The mean weight loss in the placebo group was only %3.1 [7]. Approximately 15 mg of patients using 15 mg %57’si ba\u015flang\u0131\u00e7 kilosunun en az %20’sini <\/strong>kaybetmi\u015ftir. Bu, ila\u00e7 tedavisiyle kilo kontrol\u00fcnde daha \u00f6nce \u00e7ok nadir g\u00f6rd\u00fc\u011f\u00fcm\u00fcz bir sonu\u00e7tu [7]. Bu rakamlar\u0131 daha anla\u015f\u0131l\u0131r hale getirirsek, 100 kilogram a\u011f\u0131rl\u0131\u011f\u0131nda bir hastada ortalama %20 kilo kayb\u0131 yakla\u015f\u0131k 20 kilogram<\/strong> This means that, of course, these are study averages; some people lose much more weight, and some lose less. However, in the pharmacological treatment of obesity, along with thizzpatide, %20 ve \u00fczerindeki kilo kayb\u0131 art\u0131k ger\u00e7ek\u00e7i bir hedef haline gelmi\u015ftir.<\/strong>\n<\/p>\n\n\n\n

\n The GLP-1 system affects the appetite and satiety centers in the brain, reducing hunger and helping you feel full longer after meals. It also regulates glucose metabolism via the gastrointestinal system and pancreas. The addition of the GIP receptor to the system further complicates the metabolic response. GIP plays a significant role in glucose-dependent insulin secretion and influences metabolic signals in adipose tissue and the central nervous system.\n<\/p>\n\n\n\n

\n Tirzepatide targets these two systems simultaneously:\n<\/p>\n\n\n\n

reduces appetite,
It increases the feeling of fullness.
reduces total energy intake,
It improves glucose control and
It increases insulin sensitivity.<\/strong>\n<\/p>\n\n\n\n

\n Therefore, patients using thizzpatide experience not only weight loss but also significant improvements in many cardiometabolic parameters such as waist circumference, blood pressure, triglycerides and glucose metabolism [7].\n<\/p>\n\n\n\n

\n In the extended follow-up of the SURMOUNT-1 study, individuals with obesity and prediabetes had approximately for three years<\/strong> It was monitored. At the end of 176 weeks of thizzpati treatment, significant weight loss was observed. At the highest doses, the average weight loss was approximately %23’e yakla\u015fm\u0131\u015ft\u0131r<\/strong> [8].\n<\/p>\n\n\n\n

\n Even more interesting is that in these individuals who initially had prediabetes, the risk of progressing to type 2 diabetes was drastically reduced. In the study, those who received thizzpatide had approximately the same risk of developing type 2 diabetes over a three-year period compared to placebo. %93 daha d\u00fc\u015f\u00fck <\/strong>found [8]. \n<\/p>\n\n\n\n

\n This result is one of the important reasons why we shouldn't view tirzepatide as just a weight-loss drug. Achieving significant weight loss in a person with obesity and prediabetes can also significantly alter the metabolic process leading to diabetes.\n<\/p>\n\n\n\n

\n The most common side effects of tirepatide are again related to the gastrointestinal system. Most frequently Nausea, diarrhea, constipation, vomiting, early satiety, and abdominal discomfort.<\/strong> The vast majority of gastrointestinal side effects were observed in the SURMOUNT-1 study. mild or moderate severity<\/strong> This has happened and has been observed especially during dose escalation periods [7]. At the same time, it is possible to say that the frequency and severity of side effects are much lower compared to previous GLP-1 analogs. \n<\/p>\n\n\n\n

\n Tirzepatide'a usually 2.5 mg weekly<\/strong> The reason for starting with a certain dose is not because it is a strong weight-loss dose, but to allow the gastrointestinal system to adapt to the medication. The dose is then gradually increased according to the patient's tolerance and clinical response. Here again, I do not consider reaching the maximum dose as a success criterion. If a patient is losing weight well with, for example, a dose of 5 mg or 7.5 mg, has controlled appetite, and experiences no side effects, it is not always necessary to increase the dose simply because we can reach a higher dose.\n<\/p>\n\n\n\n

\n As with semagglutide, pancreatitis is a frequently discussed topic for thizzpatide. However, current randomized controlled trials and their meta-analyses... Studies have not shown that tirzepatide significantly increases the risk of acute pancreatitis.<\/strong> In a meta-analysis evaluating approximately 9,900 patients in nine randomized trials, no statistically significant increase in the risk of pancreatitis was found with tirzepatide [11]. More recent analyses have similarly shown that pancreatitis events are very rare and there is no significant dose-response relationship. Therefore, defining tirzepatide as a \u201cpancreatitis-causing drug\u201d is not consistent with current clinical data. Of course, clinical evaluation is necessary in patients who have had pancreatitis in the past or who develop severe and persistent abdominal pain, but this is a different matter.\n<\/p>\n\n\n\n

\n One of the most interesting developments regarding tirespasticity is that we are beginning to see how weight loss affects other obesity-related diseases. A very good example of this is... It is obstructive sleep apnea. <\/strong>In SURMOUNT-OSA studies, thizzopathy not only reduced body weight in individuals with obesity and moderate-to-severe obstructive sleep apnea, but also reduced the number of apneas and hypopneas during sleep, hypoxic load and hs-CRP levels. At the same time, improvements were observed in systolic blood pressure and sleep-related symptoms of the patients [12]. \n<\/p>\n\n\n\n

\n This study beautifully illustrates why the approach to obesity treatment needs to change.\n<\/p>\n\n\n\n

\n The purpose is only "How much weight have you lost?" <\/strong>It is not. The purpose is... The question is: how much has this weight loss changed a person's metabolic and chronic disease risk?<\/strong>\n<\/p>\n\n\n\n

4- Retatrutide: The Next Generation<\/strong>\n<\/p>\n\n\n\n

\n Retatrutide is one of the new molecules currently attracting the most attention in weight loss treatments. While semaglutide targets only the GLP-1 receptor and thizzpatide targets both GLP-1 and GIP receptors, retatrutide adds a third mechanism by activating GLP-1, GIP and glucagon receptors simultaneously. Therefore, retatrutide is described as a \u201ctriple agonist\u201d, that is, a triple receptor agonist [22].\n<\/p>\n\n\n\n

\n The addition of glucagon to the system is particularly interesting. While appetite and glucose metabolism are controlled via GLP-1 and GIP, activation of the glucagon receptor creates additional effects on energy expenditure and fat metabolism. Therefore, retatrutide was developed as a treatment that aims not only to make the person eat less, but also to simultaneously alter different aspects of energy metabolism and further stimulate fat burning. \n<\/p>\n\n\n\n

\n Retatrutide It is not a drug that has yet received FDA approval.<\/strong> It is still in the research phase. However, the results from the Phase 3 program are quite strong, and the manufacturer plans to submit its FDA application in the first quarter of 2027. Therefore, if the approval process is successful, it is expected to become one of the options for obesity treatment in the near future.\n<\/p>\n\n\n\n

\n Retatrutide's first major breakthrough results came from a Phase 2 study published in the New England Journal of Medicine in 2023. In the study, which included 338 adults with obesity or overweight, retatrutide was administered once a week at varying doses [22].\n<\/p>\n\n\n\n

\n 48 hafta sonunda ortalama kilo kayb\u0131 8 mg dozunda %22.8, 12 mg dozunda ise %24.2 olarak bulunmu\u015ftur. 12 mg kullanan ki\u015filerin tamam\u0131 ba\u015flang\u0131\u00e7 kilosunun en az %5’ini, %93’\u00fc en az %10’unu ve %83’\u00fc en az %15’ini kaybetmi\u015ftir [22].\n<\/p>\n\n\n\n

\n Perhaps even more interesting is that weight loss had not yet plateaued at week 48. That is, when the study ended, the weight loss curve of patients using high doses was still continuing downwards [22]. This raises the question of how much weight loss can be achieved with longer-term treatment.\n<\/p>\n\n\n\n

\n Side effects were largely gastrointestinal side effects, which we expect from this group of drugs. Nausea, diarrhea, vomiting and constipation were among the most common complaints. Most of these were mild or moderate in severity, and using a lower starting dose helped to reduce gastrointestinal side effects [22].\n<\/p>\n\n\n\n

\n One of the most striking aspects of Retatrutide for me is its effect on fatty liver disease. Fatty liver disease associated with metabolic dysfunction, or MASLD as it is currently known, is very closely related to obesity and insulin resistance. The fat that accumulates in the liver can progress over time to inflammation, MASH, and in some patients, fibrosis and cirrhosis.\n<\/p>\n\n\n\n

\n Retatrutide’\u0131n Faz 2 \u00e7al\u0131\u015fmas\u0131n\u0131n \u00f6zel bir alt analizinde, ba\u015flang\u0131\u00e7ta karaci\u011fer ya\u011f oran\u0131 %10 veya \u00fczerinde olan 98 hasta ayr\u0131ca incelenmi\u015ftir. Karaci\u011fer ya\u011f miktar\u0131 MRI tabanl\u0131 y\u00f6ntemlerle \u00f6l\u00e7\u00fclm\u00fc\u015ft\u00fcr [23]. Sadece 24 haftal\u0131k tedaviden sonra karaci\u011fer ya\u011f miktar\u0131 8 mg retatrutide ile ortalama %81.4, 12 mg ile %82.4 oran\u0131nda azalm\u0131\u015ft\u0131r. Plasebo grubunda ise anlaml\u0131 bir de\u011fi\u015fiklik g\u00f6r\u00fclmemi\u015ftir [23].\n<\/p>\n\n\n\n

\n Daha da ilgin\u00e7 olan, 48. haftada 8 mg ve 12 mg kullanan hastalar\u0131n yakla\u015f\u0131k %90’\u0131nda karaci\u011fer ya\u011f oran\u0131n\u0131n %5’in alt\u0131na, yani \u00e7al\u0131\u015fmada normal kabul edilen seviyeye inmi\u015f olmas\u0131d\u0131r [23]. Bu sonu\u00e7 bize retatrutide’\u0131n etkisinin yaln\u0131zca tart\u0131daki kilo kayb\u0131ndan ibaret olmad\u0131\u011f\u0131n\u0131 g\u00f6steriyor. Visseral ya\u011f, ins\u00fclin direnci ve karaci\u011ferdeki ya\u011f depolanmas\u0131 gibi metabolik bozukluklar\u0131n ayn\u0131 anda hedeflenebilmesi, gelecekte bu molek\u00fcl\u00fcn sadece obezite de\u011fil MASLD ve di\u011fer metabolik hastal\u0131klar a\u00e7\u0131s\u0131ndan da \u00f6nemli bir tedavi haline gelme ihtimalini g\u00fcndeme getiriyor.\n<\/p>\n\n\n\n

\n Therefore, the importance of retatrutide may not be simply about \u201chelping you lose a little more weight.\u201d If ongoing studies confirm the initial results, it could become one of the next-generation therapies targeting obesity, visceral fat, insulin resistance, and fatty liver disease within the same metabolic framework.\n<\/p>\n\n\n\n

Comparative Weight Loss Potentials<\/strong>\n<\/p>\n\n\n\n

The graph below shows the average weight loss achievable with different slimming injections, based on scientific studies:<\/strong>\n<\/p>\n\n\n\n

\"\"<\/figure>\n\n\n\n

Health Benefits Beyond Weight Loss<\/strong>\n<\/p>\n\n\n\n

\n Semaglutide (Ozempic\u00ae and Wegovy\u00ae) and Tirzepatide (Mounjaro\u00ae and Zepbound\u00ae) <\/strong>Although these treatments were initially used only for weight loss, recent scientific studies have shown that their use reduces the risk of cardiovascular disease, decreases inflammation in the body, may play a protective role in diseases such as Alzheimer's dementia, and may even slow the progression of cancer in some cases.\n<\/p>\n\n\n\n

\n I have observed this change firsthand in my own patients. Both pre-treatment and post-treatment test results show very positive outcomes in terms of sugar metabolism, cholesterol levels, and inflammation markers.\n<\/p>\n\n\n\n

\n Kalp ve damar hastal\u0131klar\u0131 a\u00e7\u0131s\u0131ndan elimizdeki en g\u00fc\u00e7l\u00fc verilerden biri semaglutide ile yap\u0131lan SELECT \u00e7al\u0131\u015fmas\u0131d\u0131r. Bu \u00e7al\u0131\u015fmada diyabeti olmayan ancak fazla kilolu veya obez ve daha \u00f6nce kalp-damar hastal\u0131\u011f\u0131 ge\u00e7irmi\u015f 17.604 ki\u015fi takip edilmi\u015ftir. Semaglutide kullanan grupta kardiyovask\u00fcler \u00f6l\u00fcm, kalp krizi veya inmeden olu\u015fan birle\u015fik kardiyovask\u00fcler sonlan\u0131m riski plaseboya g\u00f6re yakla\u015f\u0131k %20 daha d\u00fc\u015f\u00fck bulunmu\u015ftur [13]. Bu sonu\u00e7 \u00f6zellikle \u00f6nemlidir \u00e7\u00fcnk\u00fc fayda yaln\u0131zca kan \u015fekeri y\u00fcksek diyabet hastalar\u0131nda de\u011fil, diyabeti olmayan obez bireylerde de g\u00f6sterilmi\u015ftir.\n<\/p>\n\n\n\n

\n Bu ila\u00e7lar\u0131n inflamasyon \u00fczerindeki etkileri de giderek daha fazla dikkat \u00e7ekmektedir. Semaglutide ile yap\u0131lan STEP \u00e7al\u0131\u015fmalar\u0131nda ve daha sonraki analizlerde sistemik inflamasyonun en s\u0131k kullan\u0131lan g\u00f6stergelerinden biri olan hs-CRP d\u00fczeylerinde belirgin azalma g\u00f6sterilmi\u015ftir [14,15]. \u00d6rne\u011fin SELECT verilerinde semaglutide ile hs-CRP yakla\u015f\u0131k %38 oran\u0131nda azalm\u0131\u015ft\u0131r. Daha da ilgin\u00e7 olan, bu d\u00fc\u015f\u00fc\u015f\u00fcn yaln\u0131zca kilo kayb\u0131yla a\u00e7\u0131klanamamas\u0131d\u0131r. Semaglutide tedavisiyle baz\u0131 inflamatuvar proteinlerde kilo ve HbA1c de\u011fi\u015fiminden ba\u011f\u0131ms\u0131z de\u011fi\u015fiklikler de g\u00f6sterilmi\u015ftir [16]. Bu nedenle GLP-1 temelli tedavilerin etkisinin yaln\u0131zca \u201ckilo verdikleri i\u00e7in inflamasyon azal\u0131yor\u201d \u015feklinde a\u00e7\u0131klanmas\u0131 giderek yetersiz kalmaktad\u0131r.\n<\/p>\n\n\n\n

\n There are also some very interesting results regarding neurodegenerative diseases. In real-life studies examining large patient populations with type 2 diabetes, it has been reported that the risk of receiving a first-time Alzheimer's disease diagnosis is lower in people using semaglutide compared to those using some other diabetes medications [17]. In one study, the risk of receiving an Alzheimer's diagnosis in patients using semaglutide was found to be significantly lower in those using insulin after a three-year follow-up. Larger analyses of GLP-1 receptor agonists have also shown results indicating a decrease in the incidence of dementia and other neurocognitive diseases [18,19]. \n<\/p>\n\n\n\n

\n There are several explanations for this that may also be biologically plausible. GLP-1 receptors are not only found in the pancreas and gastrointestinal system; they are also present in the central nervous system. GLP-1 signaling has been shown to influence several mechanisms thought to be important in Alzheimer's disease, such as neuroinflammation, insulin signaling, mitochondrial function, and synaptic plasticity. Obesity, type 2 diabetes, vascular disease, and chronic inflammation are themselves significant risk factors for dementia. Therefore, the fact that these drugs reduce several of these risk factors simultaneously could create a different area of application in the future prevention of neurodegenerative diseases. \n<\/p>\n\n\n\n

\n The data regarding cancer is also noteworthy. Obesity and hyperinsulinemia are associated with many types of cancer, including breast, colorectal, liver, and endometrial cancer. Therefore, weight loss, reduction in insulin resistance, and decrease in systemic inflammation could theoretically affect cancer risk and tumor biology. Recently, not only theoretical studies but also extensive real-world data have begun to emerge on this subject. In large-scale data analyses presented at the American Society of Clinical Oncology in 2026, it was reported that cancer patients using GLP-1 receptor agonists had a lower risk of metastatic progression in lung, breast, colorectal, and hepatocellular cancers [20]. In six of the seven cancer types examined, metastatic progression was lower, and in four cancer groups, this difference was statistically significant.\n<\/p>\n\n\n\n

\n The possible explanation for these findings is not just weight loss. It is being investigated whether GLP-1 signaling may have direct or indirect effects on inflammation, insulin\/IGF-related growth pathways, the immune system and the metabolism of some tumor cells. In laboratory and animal studies, there is data that GLP-1 receptor activation can suppress mechanisms associated with tumor growth and metastasis in some cancer models [21]. \n<\/p>\n\n\n\n

\n Of course, it would be appropriate to wait for more comprehensive and longer-term studies, but the initial thought in people's minds, "Will these injections harm me in the long run?", is gradually giving way to the question, "Should we consider using these injections for other ailments as well?"\n<\/p>\n\n\n\n

\n Actually, this change is very important. Semagglutide and thizzpatite are no longer being researched solely as drugs that reduce the number on the scale. Their potential effects are being investigated in very different areas such as cardiovascular disease, chronic inflammation, liver disease, sleep apnea, diabetes prevention, neurodegenerative diseases, and even cancer biology. Perhaps in the coming years, these drugs will be studied not only as drugs that reduce the number on the scale. "weight loss injections"<\/strong> That would be quite insufficient.\n<\/p>\n\n\n\n

Why Should I Get Tested Before I Start?<\/strong>\n<\/p>\n\n\n\n

\n Before starting treatment, some tests need to be done. The purpose of this is not only to assess whether the person is suitable for taking the medication, but also to investigate the underlying metabolic or hormonal causes of the weight problem, identify possible risk factors, and create a starting point for comparison before treatment.\n<\/p>\n\n\n\n

\n For example, fasting glucose, HbA1c, and fasting insulin provide information about glucose metabolism and insulin resistance; while liver and kidney function tests help us assess the overall metabolic status before treatment. Lipid profile, thyroid function, and other hormonal tests can also be added to the evaluation if necessary. Knowing these values before treatment is especially important for individuals with fatty liver disease, prediabetes, insulin resistance, or lipid disorders. This is because successful treatment should be evaluated not only by the question of "how much weight has been lost?" but also by the extent of improvement in the individual's metabolic health.\n<\/p>\n\n\n\n

\n At the same time, it's not just about deciding whether or not to start medication, or even comparing before and after results, but also about addressing any other risk factors the patient may have. The patient may have come solely for weight loss. But my goal is to move the patient from a starting point to a healthier one. Therefore, before starting treatment, I always request a comprehensive panel of tests. This panel includes:\n<\/p>\n\n\n\n

\n 1. Blood Glucose Tests (Fasting Glucose, insulin, Homa-IR and HbA1c)<\/strong>: It is done to evaluate current blood sugar levels and long-term blood sugar control. In addition, the person's insulin resistance is evaluated.\n<\/p>\n\n\n\n

\n 2. Kidney Function Tests (Creatinine, BUN, and Electrolytes)<\/strong>This helps us understand kidney function, monitor the patient's electrolyte balance, and address specific risks.\n<\/p>\n\n\n\n

3. Liver Function Tests (ALT, AST, GGT, ALP, and Total Bilirubin):<\/strong> Assessing the overall condition of the liver and biliary tract before treatment is crucial, particularly for establishing baseline values in relation to fatty liver disease (MASLD), which is frequently associated with obesity and insulin resistance. ALT and AST primarily provide information about damage to liver cells, while GGT, ALP, and bilirubin offer complementary information about the biliary tract and bile excretion by the liver. Abnormalities in these tests may also warrant further liver ultrasound or investigations if necessary.\n<\/p>\n\n\n\n

4. Thyroid Function Tests (TSH, fT4, Anti-Tg and Anti-TPO):<\/strong> Before treatment, it is important to assess thyroid function and determine if the individual has Hashimoto's thyroiditis, hypothyroidism, or another thyroid disease. This is because thyroid dysfunction can directly affect metabolism, energy levels, and weight control. The presence of Hashimoto's or other common thyroid diseases alone does not preclude the use of semagglutide or tyrospatite, and these treatments can be used provided thyroid function is properly monitored. The aim here is not to avoid GLP-1 treatment, but to identify any accompanying thyroid disease that may affect weight problems and to plan treatment according to the individual's overall metabolic status.\n<\/p>\n\n\n\n

5. Pancreatic Enzymes (Amylase and Lipase):<\/strong> Amylase and especially lipase levels can provide additional information about the pancreas and may be included in the assessment before treatment if the person has a known or suspected pancreatic disease. However, routine measurement of these enzymes is not necessary to predict the risk of pancreatitis in every patient who will be started on semagglutide or thizzpati. Evaluating risk factors such as clinical history, previous pancreatitis, gallstone history, excessively high triglycerides, and current abdominal pain is more meaningful.\n<\/p>\n\n\n\n

6. Lipid Profile (Total Cholesterol, LDL, HDL, Triglyceride, ApoB and Lp(a)):<\/strong> Since insulin resistance, high triglycerides, low HDL, and other lipid disorders are common in individuals with weight problems, a detailed assessment of the lipid profile before treatment is important. In addition to the standard lipid panel, I prefer to routinely assess ApoB and Lp(a) levels. ApoB provides complementary information about the total number of circulating atherogenic lipoprotein particles, different from LDL cholesterol, and helps in a more accurate assessment of cardiovascular risk. Lp(a), on the other hand, is a significant risk factor largely determined genetically, not seen in the classic lipid panel, and when elevated, can independently increase the risk of cardiovascular disease. Therefore, instead of only looking at LDL levels, I prefer to assess the individual's initial lipid and cardiovascular risk profile within a broader context. Monitoring changes in the lipid profile along with weight loss and improvement in metabolic health also helps us see the benefits of treatment beyond just weight gain.\n<\/p>\n\n\n\n

7. Vitamin Levels (Vitamin D, B12, and folate)<\/strong>\n<\/p>\n\n\n\n

\n Prior to treatment, assessment is conducted to identify common vitamin deficiencies and, if necessary, correct them before or during treatment. Since semagglutinin and thizzpati can significantly reduce appetite and total food intake, ensuring adequate micronutrient intake is crucial, especially in long-term treatments. Vitamin D levels are important for bone, muscle, and overall metabolic health; while B12 and folate are crucial for blood formation, the nervous system, and cellular function. Knowing about any existing deficiencies at the outset helps prevent nutritional deficiencies that may develop during weight loss and allows for the planning of appropriate support programs when needed.\n<\/p>\n\n\n\n

\n If any abnormalities are observed in these tests, further investigations may be requested.\n<\/p>\n\n\n\n

\n ***\n<\/p>\n\n\n\n

\n All information presented here is for general informational and educational purposes only. This content is not intended to diagnose any disease, provide personalized medical assessments, or initiate, modify, or discontinue any treatment.\n<\/p>\n\n\n\n

\n The information provided does not replace a doctor's examination, personal medical evaluation, or professional healthcare. Because health conditions and treatment needs vary from person to person, it is recommended that you consult your own doctor or relevant healthcare professional before starting any medication, supplement, treatment, or medical practice, or making any changes to your current treatment.\n<\/p>\n\n\n\n

\n Because medical information and scientific data can change over time, the information presented here should not be assumed to be applicable to every individual or every clinical situation.\n<\/p>\n\n\n\n

\n I wish you healthy days,\n<\/p>\n\n\n\n


Dr. Ahmet \u00d6zyi\u011fit<\/strong>, MD, MSc, PgDip, FAAMM, ABAARM
Longevity Physician<\/p>\n\n\n\n

\n Elite Research and Surgical Hospital\n<\/p>\n\n\n\n

<\/div>\n\n\n\n

Sources<\/strong>\n<\/p>\n\n\n\n

\n 1. Pi-Sunyer X, Astrup A, Fujioka K, et al. A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management.<\/em> New England Journal of Medicine. 2015;373:11-22. DOI: 10.1056\/NEJMoa1411892 \n<\/p>\n\n\n\n

\n 2. Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity.<\/em> New England Journal of Medicine. 2021;384:989-1002. DOI: 10.1056\/NEJMoa2032183. \n<\/p>\n\n\n\n

\n 3. Garvey WT, Batterham RL, Bhatta M, et al. Two-year effects of semaglutide in adults with overweight or obesity: the STEP 5 trial.<\/em> naturemedicine. 2022;28:2083-2091. DOI: 10.1038\/s41591-022-02026-4. \n<\/p>\n\n\n\n

\n 4. Rubino DM, Greenway FL, Khalid U, et al. Effect of Weekly Subcutaneous Semaglutide vs Daily Liraglutide on Body Weight in Adults With Overweight or Obesity Without Diabetes: The STEP 8 Randomized Clinical Trial.<\/em> JAMA. 2022;327:138-150.\n<\/p>\n\n\n\n

5.<\/strong> Masson W, Lobo M, Barbagelata L, et al. Acute pancreatitis due to different semaglutide regimens: An updated meta-analysis. Endocrinolog\u00eda, Diabetes y Nutrici\u00f3n. 2024. DOI: 10.1016\/j.endien.2024.03.012<\/strong>. \n<\/p>\n\n\n\n

6.<\/strong> Kushner RF, Ryan DH, Deanfield J, et al. Safety profile of semaglutide versus placebo in the SELECT study: a randomized controlled trial. Obesity. 2025;33:452\u2013462. DOI: 10.1002\/oby.24222<\/strong>.\n<\/p>\n\n\n\n

7.<\/strong> Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022;387:205-216. DOI: 10.1056\/NEJMoa2206038<\/strong>. \n<\/p>\n\n\n\n

8.<\/strong> Jastreboff AM, le Roux CW, Stefanski A, et al. Tirzepatide for Obesity Treatment and Diabetes Prevention. New England Journal of Medicine. 2025;392:958-971. DOI: 10.1056\/NEJMoa2410819<\/strong>. \n<\/p>\n\n\n\n

9.<\/strong> Aronne LJ, Sattar N, Horn DB, et al. Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults With Obesity: The SURMOUNT-4 Randomized Clinical Trial. JAMA. 2024;331:38-48. DOI: 10.1001\/jama.2023.24945<\/strong>.\n<\/p>\n\n\n\n

10.<\/strong> Tong K, et al. Gastrointestinal adverse events of tirzepatide in the treatment of type 2 diabetes mellitus: a meta-analysis and trial sequential analysis. medicine 2023.\n<\/p>\n\n\n\n

11.<\/strong> Zeng Q, Xu J, Mu X, et al. Safety issues of tirzepatide (pancreatitis and gallbladder or biliary disease) in type 2 diabetes and obesity: a systematic review and meta-analysis. Frontiers in Endocrinology. 2023;14:1214334. DOI: 10.3389\/fendo.2023.1214334<\/strong>.\n<\/p>\n\n\n\n

12.<\/strong> Malhotra A, Grunstein RR, Fietze I, et al. Tirzepatide for the Treatment of Obstructive Sleep Apnea and Obesity. New England Journal of Medicine. 2024;391:1193-1205. DOI: 10.1056\/NEJMoa2404881<\/strong>.\n<\/p>\n\n\n\n

\n 13. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes.<\/em> New England Journal of Medicine. 2023;389:2221-2232. DOI: 10.1056\/NEJMoa2307563.\n<\/p>\n\n\n\n

\n 14. Verma S, et al. Effects of once-weekly semaglutide 2.4 mg on C-reactive protein in adults with overweight or obesity: Exploratory analyzes of STEP 1, STEP 2, and STEP 3.<\/em> eClinicalMedicine. 2023.\n<\/p>\n\n\n\n

\n 15. Mosenzon O, et al. Impact of semaglutide on high-sensitivity C-reactive protein: exploratory patient-level analyzes of SUSTAIN and PIONEER randomized clinical trials.<\/em> Cardiovascular Diabetology. 2022.\n<\/p>\n\n\n\n

\n 16. Maretty L, et al. Proteomic changes upon treatment with semaglutide in people with obesity.<\/em> naturemedicine. 2025. DOI: 10.1038\/s41591-024-03355-2. \n<\/p>\n\n\n\n

\n 17. Wang W, et al. Associations of semaglutide with first-time diagnosis of Alzheimer's disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US.<\/em> Alzheimer's & Dementia. 2024. DOI: 10.1002\/alz.14313. \n<\/p>\n\n\n\n

\n 18. Cheng HW, et al. Impact of Glucagon-Like Peptide-1 Receptor Agonists on Dementia Risk in Patients With Type 2 Diabetes Mellitus.<\/em> 2025. \n<\/p>\n\n\n\n

\n 19. Xie Y, et al. Mapping the effectiveness and risks of GLP-1 receptor agonists.<\/em> Nature Medicine. 2025. \n<\/p>\n\n\n\n

\n 20. Orland MD, et al. Can GLP-1 receptor agonists mitigate cancer progression? A real-world analysis across obesity-associated malignancies.<\/em> Journal of Clinical Oncology. 2026;44(Suppl):3143. DOI: 10.1200\/JCO.2026.44.16_suppl.3143.\n<\/p>\n\n\n\n

\n 21. Temperley HC, et al. Metabolic Modulation in Cancer Care: The Potential Role of GLP-1 Receptor Agonists.<\/em> Journal of Clinical Oncology. 2026. DOI: 10.1200\/JCO-26-00062. \n<\/p>\n\n\n\n

\n 22. Jastreboff AM, Kaplan LM, Fr\u00edas JP, et al. Triple-Hormone-Receptor Agonist Retainer for Obesity \u2014 A Phase 2 Trial.<\/em> New England Journal of Medicine. 2023;389:514-526. DOI: 10.1056\/NEJMoa2301972. \n<\/p>\n\n\n\n

\n 23. Sanyal AJ, et al. Triple hormone receptor agonist retatrutide for metabolic dysfunction-associated steatotic liver disease: a randomized phase 2a trial.<\/em> naturemedicine. 2024;30:2037-2048. \n<\/p>","protected":false},"excerpt":{"rendered":"

Zay\u0131flama \u0130\u011fneleri (Ozempic, Mounjaro) Kilo vermek kendi i\u00e7erisinde bir hedef de\u011fil, daha sa\u011fl\u0131kl\u0131 bir ya\u015fam i\u00e7in bir ara\u00e7 olarak g\u00f6r\u00fclmelidir. Kilo fazlas\u0131 olan ki\u015filerin kardiyovask\u00fcler risklerinin daha y\u00fcksek oldu\u011fu, tip 2 diyabet ve metabolik sendrom gibi sa\u011fl\u0131k sorunlar\u0131n\u0131n daha s\u0131k g\u00f6r\u00fcld\u00fc\u011f\u00fc bilinen bir ger\u00e7ektir. Kilo verirken g\u00f6r\u00fcnt\u00fcm\u00fcz\u00fcn g\u00fczelle\u015fmesinin yan\u0131 s\u0131ra, biyolojik ve fizyolojik y\u00f6nden de […]<\/p>","protected":false},"author":1,"featured_media":0,"parent":612,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-6210","page","type-page","status-publish","hentry"],"blocksy_meta":[],"_links":{"self":[{"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/pages\/6210","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/comments?post=6210"}],"version-history":[{"count":7,"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/pages\/6210\/revisions"}],"predecessor-version":[{"id":6758,"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/pages\/6210\/revisions\/6758"}],"up":[{"embeddable":true,"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/pages\/612"}],"wp:attachment":[{"href":"https:\/\/www.ahmetozyigit.com\/en\/wp-json\/wp\/v2\/media?parent=6210"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}