Sandeep Das1, Dipayan Choudhuri2. 1. Reproductive Physiology and Endocrinology Laboratory, Department of Human Physiology, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura 799022, India. 2. Reproductive Physiology and Endocrinology Laboratory, Department of Human Physiology, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura 799022, India. Electronic address: dipayanchoudhuri@tripurauniv.in.
Abstract
AIMS: Dietary calcium a common nutrient of our daily diet found to have an anti-obesity effect which may also regulate insulin sensitivity but this effect and the exact mechanism remains unexplored. Therefore, we aimed to study the effect of different types of calcium diet on insulin sensitivity with respect to the changes in the adipokine secretions in high fat diet (HFD) induced obese rats. MAIN METHODS: Healthy male rats were subjected to HFD for 12 weeks to induce obesity and further exposed to a calcium deficient (0.25% Ca) HFD and calcium enriched (1.0% Ca) HFD for another 12 weeks. Thereafter, all rats were sacrificed to collect the blood, liver, adipose tissue and muscle for downstream analysis. KEY FINDINGS: Calcium enriched HFD (1.0% Ca) significantly reduced (p < 0.01) body weight, adiposity index, glucose level, insulin level, HOMA-IR, adipokines (TNF-α, IL-6, MCP-1, Leptin), hepatic lipid accumulation, hepatic macrophage infiltration, adipocyte hypertrophy and significantly increased (p < 0.01) the adiponectin level, in HFD induced obese rats. The down-regulation of the adipokine secretion significantly increased (p < 0.01) the hepatic and muscle glycogen synthase activity and suppressed the hepatic gluconeogenesis activity via activating the insulin receptor-mediated PI3K/AKT/GLUT insulin signaling pathway thereby improving the insulin sensitivity. On the other hand calcium deficient HFD (0.25% Ca) accelerated the risk of insulin resistance (IR) due to its inability to improve insulin sensitivity by activating the associated pathways. SIGNIFICANCE: Calcium enriched HFD (1.0% Ca) reduced the risk of IR by improving the hepatic and muscle insulin sensitivity by restoring adipokine secretion.
AIMS: Dietary calcium a common nutrient of our daily diet found to have an anti-obesity effect which may also regulate insulin sensitivity but this effect and the exact mechanism remains unexplored. Therefore, we aimed to study the effect of different types of calcium diet on insulin sensitivity with respect to the changes in the adipokine secretions in high fat diet (HFD) induced obeserats. MAIN METHODS: Healthy male rats were subjected to HFD for 12 weeks to induce obesity and further exposed to a calcium deficient (0.25% Ca) HFD and calcium enriched (1.0% Ca) HFD for another 12 weeks. Thereafter, all rats were sacrificed to collect the blood, liver, adipose tissue and muscle for downstream analysis. KEY FINDINGS:Calcium enriched HFD (1.0% Ca) significantly reduced (p < 0.01) body weight, adiposity index, glucose level, insulin level, HOMA-IR, adipokines (TNF-α, IL-6, MCP-1, Leptin), hepatic lipid accumulation, hepatic macrophage infiltration, adipocyte hypertrophy and significantly increased (p < 0.01) the adiponectin level, in HFD induced obeserats. The down-regulation of the adipokine secretion significantly increased (p < 0.01) the hepatic and muscle glycogen synthase activity and suppressed the hepatic gluconeogenesis activity via activating the insulin receptor-mediated PI3K/AKT/GLUT insulin signaling pathway thereby improving the insulin sensitivity. On the other hand calcium deficient HFD (0.25% Ca) accelerated the risk of insulin resistance (IR) due to its inability to improve insulin sensitivity by activating the associated pathways. SIGNIFICANCE: Calcium enriched HFD (1.0% Ca) reduced the risk of IR by improving the hepatic and muscle insulin sensitivity by restoring adipokine secretion.
Authors: Alexey A Tinkov; Paweł Bogdański; Damian Skrypnik; Katarzyna Skrypnik; Anatoly V Skalny; Jan Aaseth; Margarita G Skalnaya; Joanna Suliburska Journal: Biomolecules Date: 2021-05-04