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glucagon action is important for normal glucose homeostasis (871), and given its potent anti-insulin effects on the liver in particular, it is not surprising that an elegant and tightly controlled reciprocal paracrine regulatory system has evolved to favor either insulin or glucagon secretion, but not both, in any given metabolic state (863). it was shown in 1970 that insulin-deficient diabetes was a state of relative hyperglucagonemia and -cell hyperresponsiveness to the glucagon secretagogue arginine (861), and subsequent studies confirmed that insulin acts in a paracrine manner to suppress glucagon release from the islet (29, 280, 523, 890). insulin per se is sufficient to suppress glucagon levels during euglycemia and hypoglycemia in humans with type 1 diabetes (t1d), and fasting glucagon levels are correlated with insulin resistance in nondiabetic humans (164, 223, 756). mice lacking the insulin receptor in -cells provided direct genetic evidence for this mechanism; these mice exhibited hyperglucagonemia in the fed state and during insulin tolerance tests (393). the mechanism for insulin suppression of -cell glucagon secretion is incompletely elucidated but has been shown to involve pi3k activity and phosphodiesterase-mediated degradation of camp (213, 683). overall, the importance of glucagon in insulin action and diabetes is underappreciated (862); the inability of mice lacking the glucagon receptor to develop diabetes upon -cell destruction is only one of many striking illustrations of this (468). d. peripheral effects of cns insulin action a role for the cns in the regulation of glucose metabolism has been appreciated since the 1850s (55), but the subject has experienced a renaissance in the past 20 yr (444). insulin is transcytosed across the blood-brain barrier (40) and both neurons and glial cells express insulin receptors (652). a major function of insulin in the brain is the suppression of appetite (48, 912). neuron-specific insr deletion predisposes mice to diet-induced obesity and concomitant hepatic insulin resistance, likely through appetite modulation (104). neuron-specific rescue of insr expression in wholebody insr/ mice extends lifespan from a few days to a few weeks, although the rescued mice still develop profound diabetes, indicating that the full beneficial effects of brain insulin action require intact peripheral insulin receptors (591). indeed, cns signaling has been demonstrated to regulate hepatic insulin action through mechanisms independent of energy balance. the 2002 finding that intracerebroventricular insulin administration was sufficient to suppress hepatic glucose production in rodents (after a 1 h time delay) (588) spurred further investigation in the field. subsequently, insulin action in certain hypothalamic nuclei was reported to potently suppress hepatic glucose production (588, 653), promote muscle glucose uptake (415), suppress adipose tissue lipolysis (415, 737), and suppress glucagon secretion (612) in rodents. nasal insulin administration, which disproportionately increases cerebrospinal fluid insulin concentrations, has been shown to enhance insulin suppression of hepatic glucose production in hyperinsulinemiceuglycemic clamp studies in lean humans (308). however, a physiological increase in brain insulin levels per se is insufficient to alter hepatic glucose production in dogs (208, 675). the mechanisms linking brain and peripheral insulin action are elusive, but likely involve sympathetic and parasympathetic outflow and possibly the hypothalamus-pituitary-adrenal (hpa) axis. for example, hepatic vagotomy was shown in one study to block the effects of cns insulin on hgp (653), although the normal hepatic glucose metabolism of mice lacking hepatic muscarinic acetylcholine receptors (480) and the normal hepatic insulin action of de
في حين أن الكربوهيدرات، التي توفر الجلوكوز للجسم لدعم عملية التمثيل الغذائي، هي حاسمة للنظام الغذائي، تناول غير مناسب يمكن أن يؤدي إلى ارتفاع السكر في الدم، ونقص السكر في الدم، وتقلبات نسبة السكر في الدم التي تضر النتائج الصحية (الشكل 2). الشكل 2- الأرباح التي يمكن أن تتراوح بين 2 و 2 عواقب عدم توازن الجلوكوز. a. فرط السكر في الدم (ارتفاع مستوى السكر في الدم) قد تسهم في تعزيز الدهون والعضلات الأيض; بالإضافة إلى ذلك ، يفضل فرط السكر في الدم مضاعفات في حالات الأمراض الحادة بما في ذلك الجراحة والأمراض الخطيرة.