The role of postprandial thermogenesis in the development of impaired glucose tolerance and type II diabetes

Abstract

Accounting for 5%–15% of total daily energy expenditure, postprandial thermogenesis (PPT) refers to an acute increase in resting metabolic rate (RMR) in the hours after eating. This is largely explained by the energy costs of processing the macronutrients of a meal. Most individuals spend the majority of the day in the postprandial state, thus over one’s lifetime even minor differences in PPT may possess true clinical significance. In contrast to RMR, research indicates that PPT may be reduced in the development of both prediabetes and type II diabetes (T2D). The present analysis of existing literature has found that this impairment may be exaggerated in hyperinsulinemic-euglycemic clamp studies compared with food and beverage consumption studies. Nonetheless, it is estimated that daily PPT following carbohydrate consumption alone is approximately 150 kJ lower among individuals with T2D. This estimate fails to consider protein intake, which is notably more thermogenic than carbohydrate intake (20%–30% vs. 5%–8%, respectively). Putatively, dysglycemic individuals may lack the insulin sensitivity required to divert glucose toward storage—a more energy-taxing pathway. Accordingly, the majority of findings has associated an impaired PPT with a reduced “obligatory” energy output (i.e., the energy costs associated with nutrient processing). More recently, it has been reported that “facultative” thermogenesis [e.g., the energy costs associated with sympathetic nervous system (SNS) stimulation] may also contribute to any impairment in PPT among individuals with prediabetes and T2D. Further longitudinal research is required to truly ascertain whether meaningful changes in PPT manifest in the prediabetic state, before the development of T2D.