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GLP-1 and GIP receptor activation can buffer glucagons hyperglycemic potential through glucose-dependent insulin secretion, appetite suppression, delayed gastric emptying, and improved nutrient handling

(We see it already in the prospect of drug therapies for GLP-1-related muscle loss.) But the many clinical trials of the new obesity treatments do not and cannot look at what might happen over a decade or more of steady use, or what might happen if the injections must be discontinued after that long

[1] Primarily, semaglutide stimulates insulin secretion from the pancreas when blood glucose levels are elevated, whilst simultaneously suppressing the release of glucagon, a hormone that raises blood sugar

Your prescriber will weigh efficacy, diabetes status, and personal risk factors