Glucagon Satiety Not Preserved in Obese Diabetes Mellitus

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Glucagon-Induced Satiety Preserved in T1DM, Not Obesity
Glucagon-Induced Satiety Preserved in T1DM, Not Obesity

Glucagon increases satiety index in lean individuals and in individuals with type 1 diabetes mellitus (T1DM), but not in those with obesity, according to a study published in the Journal of Clinical Endocrinology & Metabolism.

Ayman M. Arafat, M.D., from Charité-University Medicine in Berlin, and colleagues examined glucagon-suppressive effects on circulating total- and acyl-ghrelin in obesity and T1DM in a prospective double-blind, placebo-controlled study. Endocrine and metabolic responses to intramuscular glucagon administration were assessed in 13 patients with T1DM, 11 obese adults, and 13 healthy lean controls.

The researchers found that, in T1DM and in lean participants, glucagon significantly increased satiety index, but failed to induce satiety in obese individuals. In all study groups, total-ghrelin significantly decreased after glucagon administration, and acyl-ghrelin decreased significantly in lean participants. In obese participants, acyl-ghrelin concentrations showed no change, and in T1DM participants, concentrations increased significantly. In all groups there was a positive correlation between changes in acyl-ghrelin and changes in non-estrified fatty acid concentrations.

"Glucagon-induced satiety was preserved in T1DM but not in obesity," the authors write. "This effect was unrelated to changes in total- or acylated-ghrelin and was independent upon endogenous insulin release. In contrast to the insulin-independent glucagon-induced suppression of total-ghrelin, glucagon- and/or insulin-induced modification of lipolysis may determine changes in acylated-ghrelin."

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