Glucagon-like peptide 1 (GLP-1) is secreted mainly by the intestine in a nutrient-dependent manner and stimulates glucose-induced insulin secretion, inhibits gastric emptying, food intake, and glucagon secretion. All these beneficial effects make GLP-1 as a promising, and currently in the market, drug candidate for the treatment of type 2 diabetes. More recently, it has been also demonstrated that within the central nervous system, GLP-1 also exerts important metabolic actions inhibiting food intake, increasing insulin secretion, and modulating behavioral responses. In this review, we will focus on the metabolic actions and mechanisms of the central GLP-1 system: modulation of energy intake, glucose metabolism, and fatty acid metabolism.
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http://dx.doi.org/10.1016/B978-0-12-381517-0.00011-4 | DOI Listing |
Diabetes Metab
January 2025
Division of Diabetes, Nutrition and Metabolic Disorders, CHU Liège, Liège, Belgium; Division of Clinical Pharmacology, Centre for Interdisciplinary Research on Medicines (CIRM), Liège University, Liège, Belgium. Electronic address:
Background: Obesity is an increasing public health problem because of its high prevalence and associated morbidity and mortality. Two weight-loss strategies are currently used, either bariatric surgery or pharmacological therapy with glucagon-like peptide-1 receptor agonists (GLP-1RAs). Preclinical studies in rodents suggested an increased risk of additive disorders after bariatric surgery contrasting with a reduced risk with GLP-1RAs.
View Article and Find Full Text PDFCNS Spectr
January 2025
Department of Psychiatry, University of Toronto, Toronto, ON, Canada.
Incretin-based treatments, such as glucagon-like peptide-1 receptor (GLP-1R) agonists (eg liraglutide and semaglutide), have rapidly transformed obesity treatment. The well-documented weight loss effect from these agents is considered to be primarily a result of their actions on food intake, but frequent anecdotal reports from varied sources have suggested that they might also broadly affect consummatory behavior, including alcohol and drugs of abuse, suggesting a potential modulatory effect on reward behavior. Herein, we critically review the extant literature on the behavioral effects of GLP-1R agonists in humans, including their impact on feeding behavior, alcohol/drug intake, and overall reward response.
View Article and Find Full Text PDFDiabetes Metab Syndr
January 2025
Department of Dermatology, Xiangya Hospital, Central South University, Changsha, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Hunan Engineering Research Center of Skin Health and Disease, Xiangya Hospital, Central South University, Changsha, China. Electronic address:
Objective: To investigate the causal association of using glucagon-like peptide-1 receptor (GLP1R) agonists with autoimmune diseases.
Methods: The available cis-eQTLs for drugs target genes (GLP1R) were used as genetic variants for exposure to GLP1R agonists. Type 2 diabetes was used as positive control.
Am J Gastroenterol
January 2025
Center for Health Equity Research and Promotion, VA Pittsburgh Healthcare System, Pittsburgh, PA.
Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), an increasing public health concern, remains challenging to diagnose and risk-stratify. We assessed the 1) prevalence of MASLD risk factors among Veterans in Veterans Health Administration (VA) care, 2) factors associated with MASLD diagnosis; and 3) associations between MASLD diagnosis and receipt of care.
Methods: Veterans with MASLD risk factors, including obesity, pre-diabetes, diabetes, or dyslipidemia, were identified using International Classification of Diseases-10 codes and followed in 2019-2022.
J Alzheimers Dis
January 2025
Department of Physiology and Pathophysiology, Jiaxing University Medical College, Jiaxing, China.
Alzheimer's disease (AD) is the most common disease associated with cognitive dysfunction, which is closely associated with type 2 diabetes mellitus (T2DM) in clinical manifestations, pathological changes and prevention. Inhibition of dipeptidyl peptidase 4 (DPP-4) can lower blood glucose levels by stimulating insulin secretion. Besides, it can affect cognitive function through the neuroprotective effect of DPP-4 substrates, such as glucose-dependent insulin peptide and glucagon-like peptide-1, the proteolytic effect on amyloid-β and the protective effect on neuronal structure.
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