Abstract
Glucose levels in blood must be constantly maintained within a tight physiological range to sustain anabolism. Insulin regulates glucose homeostasis via its effects on glucose production from the liver and kidneys and glucose disposal in peripheral tissues (mainly skeletal muscle). Blood levels of glucose are regulated simultaneously by insulin-mediated rates of glucose production from the liver (and kidneys) and removal from muscle; adipose tissue is a key partner in this scenario, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver when blood glucose levels are depleted. During sleep at night, the gradual development of insulin resistance, due to growth hormone and cortisol surges, ensures that blood glucose levels will be maintained within normal levels by: (a) switching from glucose to NEFA oxidation in muscle; (b) modulating glucose production from the liver/kidneys. After meals, several mechanisms (sequence/composition of meals, gastric emptying/intestinal glucose absorption, gastrointestinal hormones, hyperglycemia mass action effects, insulin/glucagon secretion/action, de novo lipogenesis and glucose disposal) operate in concert for optimal regulation of postprandial glucose fluctuations. The contribution of the liver in postprandial glucose homeostasis is critical. The liver is preferentially used to dispose over 50% of the ingested glucose and restrict the acute increases of glucose and insulin in the bloodstream after meals, thus protecting the circulation and tissues from the adverse effects of marked hyperglycemia and hyperinsulinemia.
Highlights
Introduction nal affiliationsFood has major effects on physical health
Insulin plays a primary role in glucose homeostasis via its effects on insulin-sensitive tissues: blood levels of glucose are regulated simultaneously by the rates of glucose production from the liver, and the rates of its removal from peripheral tissues
Adipose tissue is a key partner in the liver–muscle interplay, providing nonesterified fatty acids (NEFA) as an alternative fuel for skeletal muscle and liver, when blood glucose levels are depleted
Summary
The liver plays a key role in glucose homeostasis. Its main metabolic function is to store glucose as glycogen after a meal and release it into the bloodstream (via glycogenolysis and gluconeogenesis) when required to maintain a constant concentration of glucose under any circumstances [6]. But on a chronic basis cortisol and growth hormone, compete with insulin and increase hepatic glucose production through an increase in glycogenolysis and gluconeogenesis [26,27,28,29]. Adrenaline, cortisol, and growth hormone increase gluconeogenesis by an indirect mechanism, via an increase in lipolysis in adipose tissue and supply of glycerol and NEFA to the liver [30]. These effects of growth hormone and cortisol are of major importance in developing a transient insulin resistant state in the early morning hours during sleep, which helps to maintain euglycemia (see below)
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