Diabetes and Frailty. Part 1: Sarcopenia
Diabetes and Frailty. Part 1: Sarcopenia
Hormones are key regulators of human muscle metabolism, and age-related hormonal changes are important biological contributors to skeletal muscle decline, with an accelerated loss of muscle mass and frailty.
IGF-1 is decreased in diabetes, and it plays a role in the protein synthesis of the muscle because of increase proteolysis.
It has been shown that testosterone levels are low both in diabetic patients and those with metabolic syndrome. In addition, it has been described that low testosterone levels are associated with IR, and that testosterone treatment may reduce IR.
Vitamin D levels are lower in patients with diabetes than in non-diabetic individuals and, recently, it has been suggested that vitamin D deficiency may contribute to B cell dysfunction, IR and inflammation and that this may result in type 2 diabetes; small intervention studies show that vitamin D supplementation reduces systematic inflammation and improves glucose tolerance. Some, but not all studies, suggest that vitamin D levels correlate with muscle mass and strength, low levels of vitamin D are associated with falls, functional decline and the frailty syndrome.
Increased cortisol levels are also associated with sarcopaenia, although the presence of enhanced cortisol secretion in patients with type 2 diabetes is debated. It had been described that serum cortisol levels are a predictor of IR followed by IL6, TNFα, leptin and adiponectin.
Deficiency of the adipocyte hormone leptin results in hyperphagia, obesity and IR. Ghrelin could produce glucose intolerance, decreased glucose stimulated insulin secretion and reduced leptin sensitivity. This provides partial evidence that ghrelin may play an important role in regulating beta-cell function.
Hormone Imbalance
Hormones are key regulators of human muscle metabolism, and age-related hormonal changes are important biological contributors to skeletal muscle decline, with an accelerated loss of muscle mass and frailty.
IGF-1 is decreased in diabetes, and it plays a role in the protein synthesis of the muscle because of increase proteolysis.
It has been shown that testosterone levels are low both in diabetic patients and those with metabolic syndrome. In addition, it has been described that low testosterone levels are associated with IR, and that testosterone treatment may reduce IR.
Vitamin D levels are lower in patients with diabetes than in non-diabetic individuals and, recently, it has been suggested that vitamin D deficiency may contribute to B cell dysfunction, IR and inflammation and that this may result in type 2 diabetes; small intervention studies show that vitamin D supplementation reduces systematic inflammation and improves glucose tolerance. Some, but not all studies, suggest that vitamin D levels correlate with muscle mass and strength, low levels of vitamin D are associated with falls, functional decline and the frailty syndrome.
Increased cortisol levels are also associated with sarcopaenia, although the presence of enhanced cortisol secretion in patients with type 2 diabetes is debated. It had been described that serum cortisol levels are a predictor of IR followed by IL6, TNFα, leptin and adiponectin.
Deficiency of the adipocyte hormone leptin results in hyperphagia, obesity and IR. Ghrelin could produce glucose intolerance, decreased glucose stimulated insulin secretion and reduced leptin sensitivity. This provides partial evidence that ghrelin may play an important role in regulating beta-cell function.
Source...