Pancreatic beta cell function

Pancreatic beta cell function (synonyms Gβ or, if calculated from fasting concentrations of insulin and glucose, HOMA-Beta or SPINA-GBeta) is one of the preconditions of euglycaemia, i.e. normal blood sugar regulation. It is defined as insulin secretory capacity, i.e. the maximum amount of insulin to be produced by beta cells in a given unit of time. Beta cells play a paramount role in glucose homeostasis. Progressive loss of insulin secretory capacity is a key defect associated with the transition from a healthy glycaemic state to hyperglycaemia, characteristic of untreated diabetes mellitus. In type 1 diabetes mellitus and pancreatogenic diabetes beta cell destruction is a primary event from the perspective of the feedback loop. In type 2 diabetes beta cell dysfunction is an essential constituent as well, but subsequent to the development of insulin resistance. Other mechanisms, including lipotoxicity, amyloid deposition, oxidative stress, mitochondrial dysfunction, ER stress and inflammation may be involved as well. The beta cell loss in type 2 diabetes is mainly caused by reduced beta cell number rather than size. Hyperglycaemia becomes clinically significant once insulin over-secretion can no longer compensate for the degree of insulin resistance. Measuring beta-cell function is a challenge, since insulin secretory capacity cannot be readily assessed. Therefore, indirect methods of measurement have been developed. They include dynamic and static function tests. Dynamic function tests for beta-cell function include: Oral glucose tolerance testing (OGTT) Intravenous glucose tolerance tests (IVGTT) Meal tolerance tests Hyperglycaemic clamp Static function tests for the assessment of beta-cell function comprise: Insulin-glucose ratio Amended insulin-glucose ratio HOMA-Beta SPINA-GBeta Measuring beta-cell function requires the rate of secretion to be interpreted in relation to the prevailing glucose concentration. Therefore, a mathematical model is needed that links the time courses of insulin secretion and glucose concentration as a mechanistic causal relationship.

Pancreatic Sirtuin 3 Deficiency Promotes Hepatic Steatosis by Enhancing 5-Hydroxytryptamine Synthesis in Mice With Diet-Induced Obesity

Johan Auwerx, Kristina Schoonjans

Sirtuin 3 (SIRT3) is a protein deacetylase regulating beta-cell function through inhibiting oxidative stress in obese and diabetic mice, but the detailed mechanism and potential effect of beta-cell-specific SIRT3 on metabolic homeostasis, and its potential ...

AMER DIABETES ASSOC2021

The role of nicotinamide riboside metabolism in pancreatic beta cells

Pancreatic Sirtuin 3 Deficiency Promotes Hepatic Steatosis by Enhancing 5-Hydroxytryptamine Synthesis in Mice With Diet-Induced Obesity

Targeting Mitochondrial Calcium Uptake with the Natural Flavonol Kaempferol, to Promote Metabolism/Secretion Coupling in Pancreatic beta-cells

The role of nicotinamide riboside metabolism in pancreatic beta cells

Targeting Mitochondrial Calcium Uptake with the Natural Flavonol Kaempferol, to Promote Metabolism/Secretion Coupling in Pancreatic beta-cells

Pancreatic Sirtuin 3 Deficiency Promotes Hepatic Steatosis by Enhancing 5-Hydroxytryptamine Synthesis in Mice With Diet-Induced Obesity