Calcium homeostasis in diabetes mellitus

Abstract

Diabetes mellitus (DM) is becoming a lifestyle-related pandemic disease. Diabetic patients frequently develop electrolyte disorders, especially diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. Such patients show characteristic potassium, magnesium, phosphate, and calcium depletion. In this review, we discuss a homeostatic mechanism that links calcium and DM. We also provide a synthesis of the evidence in favor or against this linking mechanism by presenting recent clinical indications, mainly from veterinary research. There are consistent results supporting the use of calcium and vitamin D supplementation to reduce the risk of DM. Clinical trials support a marginal reduction in circulating lipids, and some meta-analyses support an increase in insulin sensitivity, following vitamin D supplementation. This review provides an overview of the calcium and vitamin D disturbances occurring in DM and describes the underlying mechanisms. Such elucidation will help indicate potential pathophysiology-based precautionary and therapeutic approaches and contribute to lowering the incidence of DM.

Physiological assessment of high glucose neurotoxicity in mouse and rat retinal explants

“…Regarding the effect of the HG condition on calcium signaling, previous studies have suggested an altered calcium homeostasis in diabetics animals (Ahn, Kang, & Jeung, ; Pereira et al, ; Sorrentino et al, ). In cardiomyocytes, a deregulation of Ca 2+ cycling and diminished Ca 2+ influx have been shown under diabetic conditions (Bergh, Hjalmarson, Sjögren, & Jacobsson, ; Lu et al, ; Pereira et al, ).…”

Vitamin D and cardiometabolic disorders: a review of current evidence, genetic determinants and pathomechanisms

“…Moreover, insulin release is a process dependent on calcium, and as low vitamin D levels can lead to hypocalcaemia, this can also disrupt insulin secretion . Vitamin D regulates extracellular calcium to ensure normal calcium influx, thereby enhancing insulin action and signal transduction .…”

Type 2 diabetes mellitus complicated with idiopathic hypoparathyroidism where poor glycaemic control was associated with low adherence to exercise and medication due to hypocalcaemia

“…Associations between IHP and T2DM are not well understood as IHP is a rare disease, with a period prevalence of 7.2 per million population in Japan 10. Although previous in vitro and in vivo studies have reported on the importance of extracellular calcium concentrations for insulin secretion,11–15 the insulin secretion levels following glucagon stimulation tests did not increase after the treatment of hypocalcaemia in this case (table 3); this suggested that the diabetes was not secondary to hypocalcaemia. The low PTH levels may have weakened insulin secretion in this case, as in vitro studies have shown that PTH (1–34) directly stimulates insulin release from pancreatic islets through the stimulation of cyclic adenosine monophosphate (cAMP) production or activation of protein kinase C 16 17.…”