{"id":3773,"date":"2025-11-30T20:08:18","date_gmt":"2025-11-30T20:08:18","guid":{"rendered":"https:\/\/magazines.uthscsa.edu\/schools\/?p=3773"},"modified":"2025-12-08T22:14:02","modified_gmt":"2025-12-08T22:14:02","slug":"the-incretin-revoltuion","status":"publish","type":"post","link":"https:\/\/magazines.uthscsa.edu\/schools\/2025\/11\/30\/the-incretin-revoltuion\/","title":{"rendered":"The incretin revolution"},"content":{"rendered":"

Two scientists share their reflections on a new era emerging for treatment of Type 2 diabetes and obesity<\/strong><\/span><\/h2>\n

By Claire Kowalick<\/p>\n

For people living with Type 2 diabetes and obesity, the dual challenge of controlling glucose metabolism and body weight can be challenging with previous treatments. Newly formulated drugs that mimic members of the incretin family, such as the glucagon-like peptide-1 receptor agonists (GLP-1 RAs), are changing how we think about metabolic disease.<\/p>\n

\u201cThese drugs work by regulating how the body manages glucose, and their impact has been transformational,\u201d said Peng Zhao, PhD, an assistant professor in the Department of Biochemistry and Structural Biology at the Joe R. and Teresa Lozano Long School of Medicine at The University of Texas at San Antonio’s Health Science Center.<\/p>\n

What are incretin-based drugs?<\/strong><\/span><\/h3>\n

Incretin-based drugs have been around for about two decades and include peptides that mimic the body\u2019s natural incretin hormones, particularly GLP-1 drugs, which stimulate insulin production in response to food intake. Because the peptides break down quickly in the body, these drugs require subcutaneous injection and cannot yet be formulated as pills.<\/p>\n

The earliest versions of GLP-1 RAs had short half-lives and required daily injections. Over time, pharmaceutical researchers extended the action of these drugs, now allowing for weekly dosing. Combining them with drugs like DPP-4 inhibitors, which block the breakdown of the body\u2019s natural GLP-1, further enhanced their effect.<\/p>\n

Explosion of interest in new formulas<\/strong><\/span><\/h3>\n

Interest in these drugs has exploded recently due to dual incretin family agonists like tirzepatide, which activate both GLP-1 and gastric inhibitory polypeptide (GIP) receptors. In clinical studies, these incretin-based drugs have demonstrated weight loss of up to 20% of total body weight, marking a dramatic improvement over earlier formulations.<\/p>\n

\u201cThis is important because weight loss has a much more sustained metabolic benefit than blood glucose reduction alone,\u201d said Zhao.<\/p>\n

The next generation of treatment may go even further, with triple agonist, or triagonist, drugs currently in phase 2 clinical trials that simultaneously target GLP-1, GIP and glucagon receptors. Each incretin pathway has limitations, but combination treatments may offer a more balanced metabolic effect, particularly in reducing ectopic lipid accumulation \u2014 fat stored around internal organs \u2014 which is a key driver of metabolic dysfunction.<\/p>\n

The ultimate goal of scientists developing these drugs is to make an oral version that mimics multiple incretin family hormones. Several such drugs are in clinical trials.<\/p>\n

Challenges remain for \u2018miracle\u2019 drugs<\/strong><\/span><\/h3>\n

The prohibitive cost is a main deterrent to these newer GLP-1 RAs. Without insurance, these drugs can run as high as $1,000 per month, although some manufacturers offer direct-to-patient discounts of over 60%. Side effects during early treatment, such as nausea and vomiting, can be bothersome and cause some patients to abandon treatment. Recently, reports have also emerged about the potential links between GLP-1 RAs and rare thyroid cancers and pancreatic complications. Safety studies are still needed to investigate the long-term effects of continued use of these drugs.<\/p>\n

Zhao\u2019s lab is currently investigating how these treatments affect broader metabolic pathways such as adenosine monophosphate -activated protein kinase (AMPK), a critical regulator of energy balance that is often repressed in obesity and fatty liver disease.<\/p>\n

\u201cGLP-1 RAs seem to have an indirect but strong influence on AMPK activity,\u201d Zhao said. \u201cWe are using molecular tools to explore how these treatments shift the entire gene expression profile related to energy metabolism and liver health.\u201d<\/p>\n

\u201cGLP-1 receptor agonists are among the most revolutionary therapies in the treatment of obesity.\u201d<\/span><\/p><\/blockquote>\n

\u2013 Shangang Zhao, PhD,<\/strong> assistant professor in the Department of Medicine<\/span><\/h6>\n

When the wonders cease<\/strong><\/span><\/h3>\n

What happens when people stop taking GLP-1 RA drugs, and can we make their effects last? These are the questions Shangang Zhao, PhD, assistant professor in the university\u2019s Department of Medicine, studies in his lab in what may be one of the most critical frontiers in obesity research.<\/p>\n

\u201cGLP-1 receptor agonists are among the most revolutionary therapies in the treatment of obesity,\u201d Zhao said. \u201cBut they are not the final solution.\u201d<\/p>\n

Zhao\u2019s recent studies explore how these drugs work far beyond their known ability to suppress appetite. In a mouse model, he observed that one of the most dramatic effects occurs almost immediately and happens not in the gut, but in the brain.<\/p>\n

\u201cIn the first day after taking a GLP-1 RA drug, even before losing any fat, we saw a major reduction in leptin levels,\u201d Zhao said.<\/p>\n

\u2018Less is more\u2019 when it comes to leptin<\/strong><\/span><\/h3>\n

Leptin, a hormone produced by adipocytes, or fat cells, was once thought to be the key to curing obesity after its discovery in the 1990s. Scientists initially believed increasing leptin levels could suppress appetite and reverse weight gain. However, leptin is already elevated in people with obesity, sometimes as much as 10 times higher than in people without obesity.<\/p>\n

Zhao said it appears that, instead of needing more leptin, the body becomes desensitized to the hormone. He suggests that part of the success of GLP-1 RAs comes from their ability to reduce leptin in the body, potentially by as much as 70% to 80%. He said this reduction could account for as much as half of the total effect of GLP-1 RA drugs.<\/p>\n

\u201cLess is more,\u201d Zhao said. \u201cIn several disease models, including obesity and aging, partial reduction of leptin improves glucose tolerance, reduces liver fibrosis and extends metabolic health.\u201d<\/p>\n

Diminishing returns due to adaptation<\/strong><\/span><\/h3>\n

However, once the drug is stopped, weight is rapidly regained, and mainly as fat. Zhao\u2019s studies show that while initial use of a GLP-1 RA drug might reduce body weight by up to 20%, stopping and then restarting the drug later leads to diminishing returns. During his research, subjects lost only 15% of the weight on a second round of treatment and 13% to 14% on the third round. On top of this, weight loss included fat and muscle, but the weight regained was only fat.<\/p>\n

\u201cThis is the body adapting,\u201d he said. \u201cIt has mechanisms to preserve a set intake over time. If you eat 4,000 fewer calories during treatment, your brain tries to recover that exact amount once you stop.\u201d<\/p>\n

The side effects also intensify with repeated use. Mice that tolerated the drug at first became increasingly intolerant on subsequent rounds, with more mice in each group developing severe food aversion.<\/p>\n

Zhao\u2019s lab is now investigating how to make the beneficial effects of GLP-1 RA drugs more permanent. One approach could involve combining leptin-sensitizing agents with GLP-1 RAs to amplify effects while minimizing side effects. Another might target drug tolerance and help preserve lean muscle, which is typically lost during weight reduction.<\/p>\n

While current GLP-1 RA drugs like semaglutide and tirzepatide are powerful, their impact varies widely across patients. Some individuals experience dramatic weight loss, while others experience little to none, even at higher doses.<\/p>\n

\u201cWe need to understand why,\u201d Zhao said. \u201cThe future lies in personalized treatments through biomarkers, different drug combinations and possibly even ways to extend the benefits of the drugs after stopping them.\u201d<\/p>\n

Despite their success, GLP-1 RA drugs are not the end of the story for obesity research but merely the beginning of a much longer conversation. As researchers push forward with trials of oral versions and triple-action drugs, what is evident, Zhao noted, is that these therapies are one of the most promising medical breakthroughs to date in managing the parallel epidemics of obesity and Type 2 diabetes.<\/p>\n","protected":false},"excerpt":{"rendered":"

GLP-1\u2013based incretin drugs like semaglutide and tirzepatide are transforming obesity and Type 2 diabetes care by mimicking gut hormones that regulate insulin and appetite. However, they\u2019re costly and weight often returns when treatment stops. Researchers at UT Health San Antonio are studying how to make incretin therapies longer lasting and more effective, including combining them with drugs that improve leptin sensitivity and metabolism.<\/p>\n","protected":false},"author":653,"featured_media":3810,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[12],"magazine":[22],"issue-year":[59],"featured-story":[],"class_list":["post-3773","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-research","magazine-future","issue-year-59"],"yoast_head":"\nThe incretin revolution - Magazines of the Schools at UT Health San Antonio<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/magazines.uthscsa.edu\/schools\/2025\/11\/30\/the-incretin-revoltuion\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The incretin revolution - Magazines of the Schools at UT Health San Antonio\" \/>\n<meta property=\"og:description\" content=\"GLP-1\u2013based incretin drugs like semaglutide and tirzepatide are transforming obesity and Type 2 diabetes care by mimicking gut hormones that regulate insulin and appetite. 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