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Hypothalamic neurons detect changes in circulating hormones such as leptin and insulin and put forward outputs to sustain energy and glucose homeostasis. Because leptin and insulin receptors colocalize in ~40–60% of neurons in the hypothalamus, we characterized the metabolic phenotype of mice with selective deletion of the insulin receptor (InsR) in LepR cells. LR ΔInsR  mice presented no difference in body weight and insulin levels but increased fat mass. In the light phase, LR ΔInsR  mice exhibited increased food intake, locomotor activity, carbon dioxide production, and respiratory exchange rate. These mice showed reduced fat oxidation and reduced expression of cluster of differentiation 36 and AMP-activated protein kinase-α 1  in the liver, increased glucose oxidation in the light phase, and overall reduced basal glucose levels. To verify the impact of InsR deletion in LepR cells in obesity, we generated ob/ ob InsR fl , ob/ ob LR cre , and ob/ ob LR ΔInsR  mice. The ob/ ob LR ΔInsR  mice had higher body weight, fat mass, and expression of genes related to fat metabolism in the liver. No difference in food intake despite increased neuropeptide Y and agouti-related peptide expression, and no difference in energy expenditure, fat, or glucose oxidation was found in ob/ ob LR ΔInsR  compared with LR cre  or LR ΔInsR  controls. Remarkably, basal glucose levels were reduced, and the expression of genes associated with glucose metabolism in the liver was higher. Insulin signaling in LepR cells is required for the proper fat and glucose oxidation. These effects are independent of leptin given that the leptin-deficient ob/ ob LR ΔInsR  mice also presented reduced glycemia and higher adiposity. The mechanisms underlying these responses remain to be unveiled.

Insulin signaling in LepR cells modulates fat and glucose homeostasis independent of leptin