Raptor levels are critical for β-cell adaptation to a high-fat diet in male mice.

Objective: The essential role of raptor/mTORC1 signaling in β-cell survival and insulin processing has been recently demonstrated using raptor knock-out models. Our aim was to evaluate the role of mTORC1 function in adaptation of β-cells to insulin resistant state.

Method: Here, we use mice with heterozygous deletion of raptor in β-cells (βra) to assess whether reduced mTORC1 function is critical for β-cell function in normal conditions or during β-cell adaptation to high-fat diet (HFD).

Time-dependent effects of endogenous hyperglucagonemia on glucose homeostasis and hepatic glucagon action.

Elevation of glucagon levels and increase in α cell proliferation is associated with states of hyperglycemia in diabetes. A better understanding of the molecular mechanisms governing glucagon secretion could have major implications for understanding abnormal responses to hypoglycemia in patients with diabetes and provide novel avenues for diabetes management. Using mice with inducible induction of Rheb1 in α cells (αRhebTg mice), we showed that short-term activation of mTORC1 signaling is sufficient to induce hyperglucagonemia through increased glucagon secretion.

Effects of double burden malnutrition on energetic metabolism and glycemic homeostasis: A narrative review.

Rapid changes in the food process led to greater consumption of ultra-processed foods which, associated with reduced physical activity, increased the number of overweight and obese individuals worldwide. However, in low and middle-income countries (LMICS) the growth of the obesity epidemic took place despite the high prevalence of undernutrition in children. This generated the coexistence of these two nutritional patterns, currently defined as double burden malnutrition (DBM).

Glucagon Resistance and Decreased Susceptibility to Diabetes in a Model of Chronic Hyperglucagonemia.

Elevation of glucagon levels and increase in α-cell mass are associated with states of hyperglycemia in diabetes. Our previous studies have highlighted the role of nutrient signaling via mTOR complex 1 (mTORC1) regulation that controls glucagon secretion and α-cell mass. In the current studies we investigated the effects of activation of nutrient signaling by conditional deletion of the mTORC1 inhibitor, TSC2, in α-cells (αTSC2).