Hypoglycemia compensation mechanisms in dry fasting

Abstract

Background

Dry fasting (DF) presents three primary risks: hypovolemia, hypertonicity, and hypoglycemia. The first two have been shown to be effectively compensated, and the respective mechanisms have been studied. The behavior of glucose has only been roughly described, while the hypoglycemia compensation mechanisms remain unexplored.

Objectives

Studying the glucose behavior, the hypoglycemia compensation mechanisms, and the insulin resistance during DF.

Methods

Following parameters were daily monitored in ten participants undergoing a 5-day DF: Weight, body circumferences, glucose, creatinine clearance (GFR), insulin, HOMA-IR, acetoacetate in 24-h urine, glucagon, growth hormone (GH), IGF-1, TSH, T₄, T₃, leptin, cholesterol, LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides, and the enzymes LDH, CPK, SGPT, SGOT, and γGT.

Results

Weight, body circumferences, TSH, T₃, and T₄ decreased to minima on Day 5; insulin and HOMA-IR decreased, reaching minima on Day 4; GH, cholesterol, LDL-C, and acetoacetate increased to maxima on Day 5; Glucagon, IGF-1, and GFR increased, presenting maxima on Day 4; Glucose, leptin, and triglycerides exhibited biphasic profiles with minima on Days 3, 3, and 2, respectively; HDL-C, LDH, CPK, SGPT, SGOT, and γGT showed minimal or non-significant changes.

Conclusion

A comprehensive description of glucose behavior and the hypoglycemia compensation mechanisms in DF were presented. DF decreased insulin resistance, likely by improving the blood – cell interphase, and enhanced GFR. The increase in LDL-C, tissue-protecting IGF-1, and late increase in leptin and triglycerides were unexpected. The results may inform the development of novel therapeutic approaches for obesity, metabolic syndrome, type-2-diabetes, non-alcoholic fatty liver disease, adiposity, and atheromatous diseases.