Compensatory Responses to Nutrient Imbalances
The primary objective of compensatory responses to nutrient imbalances is to re-establish physiological homeostasis. An example of a compensatory response to an excess intake is the increased secretion of insulin following ingestion of a meal high in rapidly digested and absorbed carbohydrate (high glycemic index foods). Over the short-term, this elevation in insulin is maintained until postprandial blood glucose is restored to fasting levels, usually within a few hours after the meal. When large amounts of high glycemic index foods are repeatedly consumed throughout the day, the postprandial insulin response is sustained for longer periods which will eventually promote the downregulation of insulin receptors that contributes to glucose intolerance. The compensatory response to consumption of large amounts of fat follows a similar path. Elevated postprandial triglyceride levels require secretion of large amounts of chylomicrons to transport the triglyceride load from the intestines to the liver where it is deposited, leaving behind a high concentration of chylomicron remnants. These particles are highly atherogenic with effects on arterial plaque formation similar to those of low density lipoproteins (LDL).
Other examples of compensatory responses to nutrient imbalances involve homeostatic adjustments to maintain body pools of nutrients such as what is observed when sodium intakes are excessive and when calcium intakes are inadequate. If the amount of sodium ingested exceeds renal capacity for elimination, plasma volume will expand until the excess amounts are excreted and sodium homeostasis is re-established. A temporary expansion of plasma volume triggers a compensatory increase in resistance of the peripheral microvasculature in order to maintain a steady rate of vascular perfusion through these tissues. A sustained expansion of plasma volume caused by continuous intakes of excess sodium that overwhelm renal elimination capacity may transform the compensatory increase in peripheral resistance to an increase in blood pressure and establishment of essential hypertension.
The compensatory response to imbalances in calcium homeostasis is initiated by intakes that are not sufficient to maintain plasma calcium levels. Since a critical level of calcium in plasma is an absolute requirement for normal neuromuscular activity, coagulation, and other calcium-dependent activities, short-term deficiencies in calcium intake will trigger the release of calcium from labile skeletal reserves. When these labile reserves are depleted by failure to adjust calcium consumption, bone mineral mass will be sacrificed to release structural calcium into circulation to prevent the plasma concentration from decreasing below critical levels.
