Calcium Signaling in ß-cell Physiology and Pathology: A Revisit

Abstract

Pancreatic beta (β) cell dysfunction results in compromised insulin release and, thus, failed regulation of blood glucose levels. This forms the backbone of the development of diabetes mellitus (DM), a disease that affects a significant portion of the global adult population. Physiological calcium (Ca2+) signaling has been found to be vital for the proper insulin-releasing function of β-cells. Calcium dysregulation events can have a dramatic effect on the proper functioning of the pancreatic β-cells. The current review discusses the role of calcium signaling in health and disease in pancreatic β-cells and provides an in-depth look into the potential role of alterations in β-cell Ca2+ homeostasis and signaling in the development of diabetes and highlights recent work that introduced the current theories on the connection between calcium and the onset of diabetes.

Chronic hyperglycaemia drives functional impairment of lymphocytes in diabeticINSC94Ytransgenic pigs

“…In the Jurkat T cell line, high glucose levels were shown to inhibit T cell activation via an increase in non-enzymatic glycation of concentration-regulating calcium channels and delayed specific activation of these cells with anti-CD3 monoclonal antibody (Boldizsár, Berki, Miseta, & Németh, 2002). Since alterations of calcium homeostasis were shown in various cell types of diabetic patients (Klec, Ziomek, Pichler, Malli, & Graier, 2019), insufficient calcium-mediated signalling in T cells of diabetic pigs might point to impaired PHA-induced proliferation. Thus, the immune cell calcium homeostasis of diabetic INS C94Y tg pigs merits further investigations in future studies to examine possible correlations to the impaired T cell response in the diabetic cases observed in our study.…”

Artificial Pancreas Control Strategies Used for Type 1 Diabetes Control and Treatment: A Comprehensive Analysis

“…Recent studies show that a near-normal glucose level can be achieved only when patient had their insulin administered 60 minutes before the meal [52]. Results infer that adjusting the time and the amount of insulin can be helpful in the management of the diabetes [41]. As shown in Figure 4, delayed insulin infusion before meals can be linked to greater hyperglycemia up to three hours after the meal [54].…”

“…For example, when the BG increases following food intake, β-cells sense this change in concentration, and subsequently secrete insulin into the blood. On the other hand, when blood glucose levels are low, such as following a prolonged fasting period, the release of insulin from β-cells is inhibited [41].…”

“…For example, when the BG increases following food intake, β-cells sense this change in concentration, and subsequently secrete insulin into the blood. On the other hand, when blood glucose levels are low, such as following a prolonged fasting period, the release of insulin from β-cells is inhibited [41]. Doctors have tried to help patients of T1DM to maintain their glucose values as close to the normal range as possible to delay the onset and slow the progression of long-term diabetes complications such as renal disease, retinopathy, neuropathy, and heart disease.…”

“…Conceptual overview of the glucose-stimulated insulin secretion (GSIS) and brief excerpt of glucose sensing, oxidation into adenosine triphosphate (ATP) energy equivalents, potassium-ATP (K ATP ) channels working together, leading to calcium entry and insulin exocytosis in the pancreatic β-cells (shown with red arrow flow). (Adopted from[41]). …”