Regulation of Postabsorptive and Postprandial Glucose Metabolism by Insulin-Dependent and Insulin-Independent Mechanisms: An Integrative Approach

被引:110
作者
Dimitriadis, George D. [1 ]
Maratou, Eirini [2 ,3 ]
Kountouri, Aikaterini [4 ,5 ]
Board, Mary [6 ]
Lambadiari, Vaia [4 ,5 ]
机构
[1] Natl & Kapodistrian Univ Athens, Med Sch, Sect Med, Athens 15772, Greece
[2] Natl & Kapodistrian Univ Athens, Med Sch, Dept Clin Biochem, Athens 15772, Greece
[3] Attikon Univ Hosp, Med Sch, Dept Clin Biochem, Rimini 1, Chaidari 12462, Greece
[4] Attikon Univ Hosp, Res Inst, 1 Rimini St, Haidari 12542, Greece
[5] Attikon Univ Hosp, Diabet Ctr, Dept Internal Med 2, 1 Rimini St, Haidari 12542, Greece
[6] Univ Oxford, St Hildas Coll, Oxford OX4 1DY, England
关键词
postabsorptive postprandial glucose metabolism; fasting; insulin action secretion; liver; muscle; adipose tissue; incretins; meal sequence; GLUCAGON-LIKE PEPTIDE-1; FREE FATTY-ACID; HUMAN SKELETAL-MUSCLE; GASTRIC-INHIBITORY POLYPEPTIDE; DOSE-RESPONSE CHARACTERISTICS; HEPATIC GLYCOGEN FORMATION; HUMAN ADIPOSE-TISSUE; DE-NOVO LIPOGENESIS; LOW-GLYCEMIC-INDEX; GROWTH-HORMONE;
D O I
10.3390/nu13010159
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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.
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页码:1 / 33
页数:33
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