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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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GLP-2 prevents antipsychotics-induced metabolic dysfunction in mice.

Yanmin Peng1,2, Chenzhang Feng3,4, Shiyu Peng5,6

  • 1Shanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ameepeng@gmail.com.

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Glucagon-like peptide 2 analogue teduglutide prevents antipsychotic side effects like hypothermia and weight gain in mice. This peptide activates specific brain neurons, offering a potential treatment for metabolic dysfunction caused by antipsychotic drugs.

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Antipsychotic medications can cause severe metabolic side effects, including hypothermia and weight gain.
  • Current treatments for these side effects are lacking or ineffective for long-term management.

Purpose of the Study:

  • To investigate the potential of a glucagon-like peptide 2 (GLP-2) analogue, teduglutide, in mitigating antipsychotic-induced metabolic side effects.
  • To elucidate the underlying neural mechanisms of these side effects and teduglutide's therapeutic action.

Main Methods:

  • Utilized a mouse model to assess the effects of olanzapine (an antipsychotic) and teduglutide.
  • Investigated the role of ventromedial hypothalamus prodynorphin-expressing neurons (VMHPdyn neurons) using selective ablation and chemogenetics.
  • Measured body temperature, weight gain, glucose tolerance, and insulin sensitivity.

Main Results:

  • Teduglutide effectively prevented olanzapine-induced hypothermia and weight gain in mice.
  • Teduglutide restored glucose tolerance and insulin sensitivity.
  • Olanzapine suppressed VMHPdyn neurons, while teduglutide activated them; VMHPdyn neuron manipulation mimicked or reversed olanzapine's metabolic effects.

Conclusions:

  • VMHPdyn neurons are critical mediators of antipsychotic-induced metabolic dysfunction.
  • GLP-2 receptor agonism, via teduglutide, represents a promising therapeutic strategy to counteract acute and chronic metabolic side effects of antipsychotics.