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Obesity is a condition in which excess fat has accumulated in the body, such that it can have an adverse effect on health. Obesity is defined as a body mass index (BMI) of greater than 30 kg/m2.
Mounting evidence, including the recent (and unprecedented) phase 2 data on retatrutide, supports a role for incretin hormone agonists in treating obesity. But with great power comes great responsibility.
Glucagon-like peptide 1 (GLP-1) controls insulin secretion and body weight through activation of its receptor, GLP1R. Large-scale functional analysis of 60 GLP1R genetic variants revealed that loss-of-function (LoF) phenotypes, in particular of cell surface expression, are associated with impaired glucose control and increased adiposity.
Sa et al. identified a distinct neuronal subpopulation that controls brown adipose tissue thermogenesis. In mice fed a high-fat diet, hypothalamic GABRA5 neurons are deactivated by GABA released by surrounding astrocytes and inhibition of GABA synthesis ameliorates diet-induced obesity.
A common East Asian-specific defect of an alcohol metabolizing enzyme (ALDH2) causes glucose abnormality, obesity, and fatty liver. Here, the authors show an ALDH2 activator can treat these metabolic disorders in mice.
In mice, lipoamino acids activate the peroxisome proliferator-activated receptor alpha, thus reducing the rewarding properties of palatable food, dopamine neuron firing and the obesogenic effect of a high-fat diet.
Produce prescriptions improved fruit and vegetable intake, reduced food insecurity and improved biomarkers of cardiometabolic health, according to a large, retrospective, US-based study.
Mounting evidence, including the recent (and unprecedented) phase 2 data on retatrutide, supports a role for incretin hormone agonists in treating obesity. But with great power comes great responsibility.
In patients with heart failure (HF) with preserved ejection fraction and obesity, treatment with the glucagon-like peptide 1 receptor agonist semaglutide (2.4 mg) leads to large reductions in HF-related symptoms and physical limitations, improves exercise function and decreases body weight compared with placebo, according to the STEP-HFpEF trial.
Glucagon-like peptide 1 (GLP-1) controls insulin secretion and body weight through activation of its receptor, GLP1R. Large-scale functional analysis of 60 GLP1R genetic variants revealed that loss-of-function (LoF) phenotypes, in particular of cell surface expression, are associated with impaired glucose control and increased adiposity.
