Impact of postprandial glycaemia on health and prevention of disease

Abstract

Postprandial glucose, together with related hyperinsulinemia and lipidaemia, has been implicated in the development of chronic metabolic diseases like obesity, type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). In this review, available evidence is discussed on postprandial glucose in relation to body weight control, the development of oxidative stress, T2DM, and CVD and in maintaining optimal exercise and cognitive performance. There is mechanistic evidence linking postprandial glycaemia or glycaemic variability to the development of these conditions or in the impairment in cognitive and exercise performance. Nevertheless, postprandial glycaemia is interrelated with many other (risk) factors as well as to fasting glucose. In many studies, meal-related glycaemic response is not sufficiently characterized, or the methodology with respect to the description of food or meal composition, or the duration of the measurement of postprandial glycaemia is limited. It is evident that more randomized controlled dietary intervention trials using effective low vs. high glucose response diets are necessary in order to draw more definite conclusions on the role of postprandial glycaemia in relation to health and disease. Also of importance is the evaluation of the potential role of the time course of postprandial glycaemia.

Figure 1

Putative relationships between postprandial glycaemia and risk factors for obesity, diabetes and cardiovascular disease. FFA, free fatty acid.

Figure 2

Glucagon-like peptide-1 (GLP-1) increase insulin secretion lowers blood glucose and inhibits appetite. The ingestion of food promotes the release of GLP-1 from L-cells in the intestine, which activates vagal afferents. Activated GLP-1 neurons of the nucleus of the solitary tract (NTS) project to the hypothalamic arcuate nucleus (ARC), to modulate vagal motor outflow to the pancreas and other tissues not depicted, increasing insulin secretion from the β-cells in states of hyperglycaemia and suppresses glucagon from the α-cells, leading to lowering of blood glucose. Systemic GLP-1 may also access the brain via leaks in the blood–brain barrier such as the subfornical organ and the area postrema, as demonstrated to occur in rats. In the brain, release of GLP-1 within the NTS and from projections of GLP-1 neurons to the paraventricular neurons (PVN) leads to GLP-1-R activation, which promotes satiety and anorexia. Besides from the actions depicted in the picture GLP-1 has numerous other actions including slowing gastric emptying and thereby flattening glucose excursions, as well as cardiac effects. Adapted from Torekov et al., Obesity Reviews 2011 , and Williams, Endocrinology. 2009; 150: 2997–3001 .