Pathogenesis of fasting and postprandial hyperglycemia in type 2 diabetes: implications for therapy.
Pathogenesis of fasting and postprandial hyperglycemia in type 2 diabetes: implications for therapy.
复制标题
作者：
Rizza RA
这项研究的目的是为了更好地了解2型糖尿病患者空腹和餐后高血糖的原因。2型糖尿病患者进食前内源性葡萄糖分泌过多，进食后不能适当抑制。这在一定程度上是由于胰岛素诱导的内源性葡萄糖产生抑制受损，这在2型糖尿病的早期发展中被观察到。糖异生率的增加和糖原溶解可能导致肝脏胰岛素抵抗。胰岛素诱导的肝脏葡萄糖摄取和肝糖原合成的刺激在2型糖尿病患者中减少，主要是由于肝葡萄糖激酶激活不足导致细胞外葡萄糖摄取减少。胰岛素分泌延迟导致葡萄糖峰值浓度升高，特别是当胰高血糖素抑制受损时，而胰岛素抵抗延长高血糖持续时间，当肝脏和肝外胰岛素抵抗存在时，这可以被标记。这些研究以及许多其他研究者的研究的前提是，了解2型糖尿病的发病机制将使针对特定个体纠正特定代谢缺陷的靶向治疗的发展成为可能。我和其他许多研究人员都相信，如果每个人都接受相同的治疗，不管他们的高血糖的潜在原因是什么，这种治疗方法可能更有效，风险更低。虽然我们还没有足够的知识来真正个性化治疗，但在我看来，这种方法在不久的将来将成为常态。
The objective of this research is to gain a greater understanding of the cause of fasting and postprandial hyperglycemia in people with type 2 diabetes. Endogenous glucose production is excessive before eating and fails to appropriately suppress after eating in people with type 2 diabetes. This is due in part to impaired insulin-induced suppression of endogenous glucose production, which is observed early in the evolution of type 2 diabetes. Increased rates of gluconeogenesis and perhaps glycogenolysis contribute to hepatic insulin resistance. Insulin-induced stimulation of hepatic glucose uptake and hepatic glycogen synthesis are reduced in people with type 2 diabetes primarily due to decreased uptake of extracellular glucose presumably because of inadequate activation of hepatic glucokinase. Delayed insulin secretion results in higher peak glucose concentrations particularly when suppression of glucagon is impaired, whereas insulin resistance prolongs the duration of hyperglycemia, which can be marked when both hepatic and extra-hepatic insulin resistance are present. The premise of these studies, as well as those performed by many other investigators, is that an understanding of the pathogenesis of type 2 diabetes will enable the development of targeted therapies that are directed toward correcting specific metabolic defects in a given individual. I, as well as many other investigators, believe that such therapies are likely to be more effective and to have a lower risk than would occur if everyone were treated the same regardless of the underlying cause of their hyperglycemia. While we do not yet have sufficient knowledge to truly individualize therapy, in my opinion this approach will be the norm in the not too distant future.
登录
查看更多内容
DOI：
10.1152/ajpendo.00549.2003
发表时间：
2004-07-01
影响因子：
5.1
作者：
Basu, R;Schwenk, WF;Rizza, RA
通讯作者：
Rizza, RA
影响因子：
9.8
作者：
CAMPBELL, PJ;MANDARINO, LJ;GERICH, JE
通讯作者：
GERICH, JE
影响因子：
15.9
作者：
Basu, A;Alzaid, A;Rizza, RA
通讯作者：
Rizza, RA
影响因子：
7.7
作者：
Boden, G;Chen, XH;Mozzoli, M
通讯作者：
Mozzoli, M
影响因子：
7.7
作者：
Basu, Rita;Chandramouli, Visvanthan;Rizza, Robert A.
通讯作者：
Rizza, Robert A.