The interrelationship between sleep, diet, and glucose metabolism

Abstract

Obesity and type 2 diabetes (T2D) are increasingly common worldwide. While these disorders have increased in prevalence over the past several decades, there has been a concomitant reduction in sleep duration. Short sleep duration has been associated with higher rates of obesity and T2D, and the causality of these associations and their directionality, continue to necessitate evaluation. In this review we consider the evidence that sleep is an intrinsic factor in the development of obesity and chronic metabolic disorders, such as insulin resistance and T2D, while evaluating a potential bi-directional association. We consider the evidence that diet and meal composition, which are known to impact glycemic control, may have both chronic and acute impact upon sleep. Moreover, we consider that postprandial nocturnal metabolism and peripheral glycemia may affect sleep quality. We propose putative mechanisms whereby acute effects of nighttime glucose excursions may lead to increased sleep fragmentation. We conclude that dietary manipulations, particularly with respect to carbohydrate quality, may confer sleep benefits. Future research may seek to evaluate the effectiveness of synergistic nutrient strategies to promote sleep quality, with particular attention to carbohydrate quality, quantity, and availability as well as carbohydrate to protein ratio.

Keywords: Diet; Energy balance; Food intake; Glucose; Obesity; Orexin; Type 2 diabetes.

Figure 1.

Simplified illustration of the ‘Energy balance model’ and the ‘Carbohydrate – insulin model’ of obesity. 1a. The energy balance model proposes that changes in the food environment as well as internal signals (hormones) driven by food intake, are cues to the brain which lead to increased food intake. These signals are integrated in the brain modulating behavour reinforcing of food reward, appetite which leads to more food intake and circulating fuels. Circulating fuels and signals (e.g. leptin) indicate the energy status of various organs and are sensed by the brain to control food intake. Overall this model proposes that a genetic variation in the handling of these different processes, particularly those in the brain, are responsible for the susceptibility to develop obesity. 1b. The carbohydrate- insulin model proposes that rapid absorption of glucose after consumption of a high-GL meal increases secretion of insulin to glucagon ratio, and elicits a glucose-dependent insulinotropic polypeptide (GIP)-dominant incretin response. These inputs and/or higher insulin sensitivity in adipose tissue vs. liver or muscle lead to increased lipogenesis and fat storage. The sharp insulin response and decline in blood glucose, possibly below baseline is interpreted in the brains as a state of “cellular semistarvation” and responds with a counter-regulatory hormone response and hunger and cravings for high-GL foods. Energy expenditure may also decline related to decreased fuel availability. Overall, this model proposes that fat storage due to high insulin sensitivity and cellular semistarvation lead to obesity. GI; gastrointestinal; GIP; glucose-dependent insulinotropic polypeptide; GL, glycemic load.

Figure 2.

Transport and metabolism of dietary Trp in the CNS. Trp is derived from dietary protein along with other LNAAs. Transport of Trp/ LNAAs compete at Large Neutral Amino Acid Transporter (LAT1) sites. CHO ingestion leads to insulin secretion and dietary fat increases CCK which may also induce insulin secretion. Elevated insulin drives LNAA into muscle tissue excluding Trp. Trp transport into the brain is thus upregulated. In the brain Trp is metabolized to serotonin and melatonin or is metabolized via the kynurenine pathway. In individuals with obesity-induced inflammation leading to IR, the kynurenine pathway is upregulated. Diagram adapted from Cheon & Kim (67) CCK, cholecystokinin; CHO, carbohydrate; CNS, central nervous system; IDO, indolamine-2,3-dioxygenase; IR, insulin resistance; Trp; Tryptophan; LAT1, large neutral amino acid transporter 1; LNAA, large neutral amino acids.