Utilization of dietary glucose in the metabolic syndrome

Abstract

This review is focused on the fate of dietary glucose under conditions of chronically high energy (largely fat) intake, evolving into the metabolic syndrome. We are adapted to carbohydrate-rich diets similar to those of our ancestors. Glucose is the main energy staple, but fats are our main energy reserves. Starvation drastically reduces glucose availability, forcing the body to shift to fatty acids as main energy substrate, sparing glucose and amino acids. We are not prepared for excess dietary energy, our main defenses being decreased food intake and increased energy expenditure, largely enhanced metabolic activity and thermogenesis. High lipid availability is a powerful factor decreasing glucose and amino acid oxidation. Present-day diets are often hyperenergetic, high on lipids, with abundant protein and limited amounts of starchy carbohydrates. Dietary lipids favor their metabolic processing, saving glucose, which additionally spares amino acids. The glucose excess elicits hyperinsulinemia, which may derive, in the end, into insulin resistance. The available systems of energy disposal could not cope with the excess of substrates, since they are geared for saving not for spendthrift, which results in an unbearable overload of the storage mechanisms. Adipose tissue is the last energy sink, it has to store the energy that cannot be used otherwise. However, adipose tissue growth also has limits, and the excess of energy induces inflammation, helped by the ineffective intervention of the immune system. However, even under this acute situation, the excess of glucose remains, favoring its final conversion to fat. The sum of inflammatory signals and deranged substrate handling induce most of the metabolic syndrome traits: insulin resistance, obesity, diabetes, liver steatosis, hyperlipidemia and their compounded combined effects. Thus, a maintained excess of energy in the diet may result in difficulties in the disposal of glucose, eliciting inflammation and the development of the metabolic syndrome

Alleviation of Hyperglycemia Induced Vascular Endothelial Injury by Exenatide Might Be Related to the Reduction of Nitrooxidative Stress

“…The main contribution made in the present study is that the alleviation of hyperglycemia induced vascular endothelial injury by exenatide might be related to the inhibition of nitrooxidative stress. Insulin resistance is the main initial and independent risk factor for type 2 diabetes mellitus [ 30 ], which is usually associated with obesity, and can be induced by long-term high fat or/and high glucose diet [ 31 , 32 ]. In this study, we fed the rats with high fat emulsion in order to induce insulin resistance.…”

Adipogenesis in Different Body Depots and Tumor Development

“…Also, an intermediate adipocyte profile characterizes beige or "brite" adipocytes, which represent an inducible form of thermogenic adipocytes sporadically residing within WAT (Bukowska et al, 2018;Schoettl et al, 2018). Although both WAT and BAT adipocytes can store large amounts of lipids, their main functional differences relate to the higher oxidative capacity and energy expenditure by BAT under nervous/endocrine control (Alemany, 2011). While BAT depots are primarily found in rodent and human infants, their increased activity in adults can be demonstrated upon cold exposure, noradrenergic and pharmacological stimulation, or fasting.…”

Type 2 diabetic patients and their offspring show altered parameters of iron status, oxidative stress and genes related to mitochondrial activity

“…Le Blanc Á P. Villarroel Á V. Candia Á M. Arredondo (&) Laboratorio de Micronutrientes, Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, El Líbano 5524, Macul, Santiago, Chile e-mail: marredon@inta.uchile.cl insulinaemia, favoring the deposition of fat, increasing the circulating lipids and induces inflammation (Alemany 2011).…”