Adjustment to dietary energy availability: from starvation to overnutrition

Abstract

Humans have evolved into efficient survivors, able to bridge periods of scarcity between times of food availability. Adaptation to these changes requires specific adaptations and the establishment of metabolic priorities. These include thermal homoeostasis, maintained tissue glucose availability and the selective utilization of energy substrates, depending on their availability. A consequence of these requirements is the necessary maintenance of body reserves of energy, largely triacylglycerols, controlled by an effective ponderostat system. Body triacylglycerol reserves are used to sustain most of the body’s energy needs in periods of scarcity. Protein, throughout evolution, has been difficult to obtain, and, as a consequence, it is not used as an energy substrate except under conditions of excess, but (also) as a source of glucose and energy. Under excess energy conditions (as found in many present-day diets), the finely tuned mechanisms to survive starvation are inadequate to eliminate this excess. Humans are essentially unprepared for sustained excess energy intake; thermogenesis, increased protein turnover, growth and lipid accretion help decrease the energy burden. However, in the long-term, excess lipid accumulation in adipose tissue elicits inflammation and immune system-derived responses that deeply affect the control of energy partition, including the ponderostat setting and the disposal of excess glucose and amino acids. These changes alter the function of white adipose tissue, muscle, liver and the intestine (including the microbiota), all subjected to a low-key inflammation condition that alters their function and elicits a number of associated diseases constituting metabolic syndrome. In summary, it is hypothesized that dietary plentifulness and the pre-established mechanisms to fight scarcity are both responsible for the development of metabolic syndrome, which can be thus defined as a disease of affluence.