Abstract
The influence of alpha and beta cells, through glucagon and insulin, on energy metabolism is well known. The insulin:glucagon ratio (IGR) is a frequently discussed entity in the medical literature. However, in recent years, focus has shifted to other pathways and markers of health and disease. This communication revisits the insulin:glucagon bipolar axis and describes the significance of the IGR. It reviews the effects of various glucose-lowering drugs on this ratio, and hypothesizes that the ratio can be used to predict the appropriate choice of drugs for managing diabetes. Drugs which increase the IGR may be beneficial in insulinopenic conditions, while those which decrease IGR may be of help in the setting of hyperinsulinemia or insulin resistance.
Highlights
The influence of alpha and beta cells, through glucagon and insulin, on energy metabolism is well known
Though Defronzo [3] included the alpha cell as part of the ominous octet, and Schwartz et al [4] list it as one of the egregious eleven, less attention has been paid to this pathophysiologic player. Some reasons for this may be the multitude of factors which affect insulin and glucagon secretion, their highly variable concentrations, the existence of a significant, and variable, porto-systemic gradient, and the difficulty involved in estimating them
Beta-cell secretory capacity is known to fall with increasing duration of diabetes, so insulin levels may vary depending upon diabetes stage
Summary
Glucagon and insulin are two opposing hormones which work in tandem to maintain a normal fuel balance. By modulating the relative concentrations of glucagon and insulin, the alpha and beta cells of the pancreas control endogenous glucose production, triacylglycerol deposition, and protein synthesis [1]. Glucagon acts as a catabolic hormone, while insulin exerts anabolic effects on the body. A low insulin:glucagon ratio (IGR) stimulates mobilization of stored nutrients, increases glycogenolysis and gluconeogenesis, and promotes the breakdown of adipose tissue into free fatty acids and glycerol. A high IGR encourages biosynthesis of proteins, inhibits the production of glucose, and reduces free fatty acid release [2]. Increased (more substrate glycerol 3 phosphate and nicotinamide adenine dinucleotide phosphate (NADPH); activation of acetyl CoA carboxylase)
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