Angiotensin II in Type 2 Diabetes Mellitus

被引:45
作者
Chu, Kwan Yi [1 ]
Leung, Po Sing [1 ]
机构
[1] Chinese Univ Hong Kong, Dept Physiol, Fac Med, Shatin, Hong Kong, Peoples R China
关键词
Angiotensin II; diabetes; insulin; resistance; endocrine; pancreas; beta-cell; apoptosis; muscle; adipose; liver; CONVERTING-ENZYME-INHIBITOR; HUMAN ADIPOSE-TISSUE; BETA-CELL FUNCTION; HEPATIC STELLATE CELLS; HUMAN SKELETAL-MUSCLE; CHRONIC HEART-FAILURE; ECTOPIC FAT STORAGE; ISLET BLOOD-FLOW; INSULIN-RESISTANCE; RECEPTOR ANTAGONIST;
D O I
10.2174/138920309787315176
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Angiotensin II (Ang II) is well-known as a systemic vasoconstrictor but recently a novel role for the peptide in endocrine function has been suggested and it has been linked to the pathophysiology of type 2 diabetes mellitus. According to several large-scale clinical studies, blocking Ang II prevented the onset of type 2 diabetes in potential patients. Type 2 diabetes is a complicated disease that is primarily characterized by insulin resistance and relative insulin deficiency mediated by numerous organs. Among these organs, the pancreas, adipose tissue, skeletal muscle and liver are the most prominent in maintaining glucose homeostasis. Interestingly, locally generated Ang II has been identified in these organs, where it plays different physiological roles and is produced in relatively high amounts with significant function. In type 2 diabetic human patients or animal models, Ang II, its generating enzymes and receptors are up-regulated and trigger detrimental effects. Moreover, Ang II seems to play roles in the regulation of insulin secretion by the pancreatic beta-cell and insulin sensitivity by peripheral tissues, which are two critical factors contributing to the development of type 2 diabetes. Accordingly, inhibiting Ang II produced beneficial effects on individual organs and throughout the body. Therefore, the present review discusses the role of Ang II in particular organs during normal physiological conditions as well as in type 2 diabetes.
引用
收藏
页码:75 / 84
页数:10
相关论文
共 153 条
[1]
Active fragments of angiotensin II: Enzymatic pathways of synthesis and biological effects [J].
Ardaillou, R .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 1997, 6 (01) :28-34
[2]
ATEF N, 1994, DIABETOLOGIA, V37, P677, DOI 10.1007/s001250050163
[3]
Activated human hepatic stellate cells express the renin-angiotensin system and synthesize angiotensin II [J].
Bataller, R ;
Sancho-Bru, P ;
Ginès, P ;
Lora, JM ;
Al-Garawi, A ;
Solé, M ;
Colmenero, J ;
Nicolás, JM ;
Jiménez, W ;
Weich, N ;
Gutiérrez-Ramos, JC ;
Arroyo, V ;
Rodés, J .
GASTROENTEROLOGY, 2003, 125 (01) :117-125
[4]
BAUER PH, 1991, MOL PHARMACOL, V39, P579
[5]
Role of the adipocyte, free fatty acids, and ectopic fat in pathogenesis of type 2 diabetes mellitus: Peroxisomal proliferator-activated receptor agonists provide a rational therapeutic approach [J].
Bays, H ;
Mandarino, L ;
DeFronzo, RA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (02) :463-478
[6]
BDALLA S, 2001, J BIOL CHEM, V276, P39721
[7]
Identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARγ-modulating activity [J].
Benson, SC ;
Pershadsingh, HA ;
Ho, CI ;
Chittiboyina, A ;
Desai, P ;
Pravenec, M ;
Qi, NN ;
Wang, JM ;
Avery, MA ;
Kurtz, TW .
HYPERTENSION, 2004, 43 (05) :993-1002
[8]
Angiotensin II causes weight loss and decreases circulating insulin-like growth factor I in rats through a pressor-independent mechanism [J].
Brink, M ;
Wellen, J ;
Delafontaine, P .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (11) :2509-2516
[9]
ANGIOTENSIN-II INCREASES GLUCOSE-UTILIZATION DURING ACUTE HYPERINSULINEMIA VIA A HEMODYNAMIC MECHANISM [J].
BUCHANAN, TA ;
THAWANI, H ;
KADES, W ;
MODRALL, JG ;
WEAVER, FA ;
LAUREL, C ;
POPPITI, R ;
XIANG, A ;
HSUEH, W .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (02) :720-726
[10]
NEPHRECTOMY, CONVERTING-ENZYME INHIBITION, AND ANGIOTENSIN PEPTIDES [J].
CAMPBELL, DJ ;
KLADIS, A ;
DUNCAN, AM .
HYPERTENSION, 1993, 22 (04) :513-522