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
Highlights
This review is focused on the fate of dietary glucose under conditions of chronically high energy intake, evolving into the metabolic syndrome
The body has to find ways to circumvent the strict glucose preservation measures painstakingly developed and established through evolution for its own protection, such as insulin resistance [23,24]. These processes and effects are shown as both homoeostatic control systems and pathogenic mechanisms in the development of the metabolic syndrome, Excess glucose and insulin resistance After insulin resistance denies its entry to muscle, and decreased blood flow restricts adipose tissue uptake, most of the remaining glucose could only be used in significant amounts by brown adipose tissue (BAT) [25], or by the liver, the intestine and -perhaps- by the microbiota
Excess energy intake is primarily countered by the normal homeostatic mechanisms regulating body weight: signals eliciting a decrease in food intake combined with increased energy expenditure, i.e. higher thermogenesis, increased metabolic activity, decreased overall metabolic efficiency, and, increased energy storage
Summary
Excess energy intake is primarily countered by the normal homeostatic mechanisms regulating body weight: signals eliciting a decrease in food intake combined with increased energy expenditure, i.e. higher thermogenesis, increased metabolic activity (including enhanced protein turnover), decreased overall metabolic efficiency (which may be considered part of the thermogenic process), and, increased energy storage. Often the consequence of high-energy diets rich in fats, compound the already high digestive process-generated availability of glucose by eliciting insulin resistance. The large excess of glucose generated is largely used to promote energyconsuming processes and may result, in a significant part, converted to lipid for storage; or, in the case of coexistent high dietary fat, used for immediate disposal to prevent hyperglycemia. Even this process has limits and excess glucose damages the liver-adipose tissue energy-maintenance axis, which extends to the whole body because of the implication of defense mechanisms that inadequately try to prevent these damages. List of abbreviations WAT: white adipose tissue; BAT: brown adipose tissue; MS: metabolic syndrome
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