Relationship between insulin resistance and renin-angiotensin-aldosterone system in type 2 diabetes mellitus

doi:10.3877/cma.j.issn.1674-0785.2017.12.006

Abstract

Abstract:

Type 2 diabetes mellitus (T2DM) is a disease related to over-consumption of high-calorie foods, lack of exercise, and obesity. Insulin resistance is a state that tissue or cell responsiveness to insulin decreases. Previous studies have found that the renin-angiotensin aldosterone system (RAAS) is involved in the development of T2DM. Angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor antagonists (ARB) can delay the progression of insulin resistance, but the underlying mechanisms are still unclear. This paper reviews the recent progress in the understanding of the relationship between insulin resistance and the RAAS in T2DM.

Key words: Type 2 diabetes mellitus, Insulin resistance, Angiotensin, Aldosterone, Insulin signaling

Cuiyao Mo, Yunfeng Liu. Relationship between insulin resistance and renin-angiotensin-aldosterone system in type 2 diabetes mellitus[J]. Chinese Journal of Clinicians(Electronic Edition), 2017, 11(12): 1942-1945.

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References 19

[1]	Folli F, Kahn CR, Hansen H, et al. Angiotensin II inhibits insulin signaling in aortic smooth muscle cells at multiple levels. A potential role for serine phosphorylation in insulin/angiotensin II crosstalk [J]. J Clin Invest, 1997, 100(9): 2158-2169.
[2]	Motley ED, Eguchi K, Gardner C, et al. Insulin-induced Akt activation is inhibited by angiotensin II in the vasculature through protein kinase C-alpha [J]. Hypertension, 2003, 41(3 Pt 2): 775-780.
[3]	Simon F, Varela D, Cabello-Verrugio C, et al. Oxidative stress-modulated TRPM ion channels in cell dysfunction and pathological conditions in humans [J]. Cell Signal, 2013, 25(7): 1614-1624.
[4]	Wei Y, Sowers JR, Clark SE, et, al. Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-kappaB activation via NADPH oxidase [J]. Am J Physiol Endocrinol Metab, 2008, 294(2): E345-351.
[5]	Csibi, Communi D, Muller N, et al. Angiotensin II inhibits insulin-stimulated GLUT4 translocation and Akt activation through tyrosine nitration-dependent mechanisms [J]. PLoS One, 2010, 5(4): e10070.
[6]	Diamond-Stanic MK, Henriksen EJ. Direct inhibition by angiotensin Ⅱ of insulin-dependent glucose transport activity in mammalian skeletal muscle involves a ROS-dependent mechanism [J]. Arch Physiol Biochem, 2010, 116(2): 88-95.
[7]	Blair AB, Hajduch E, Litherland GJ, et, al. Regulation of glucose transport and glycogen synthesis in L6 muscle cells during oxidative stress. Evidence for cross-talk between the insulin and SAPK2/p38 mitogen-activated protein kinase signaling pathways [J]. J Biol Chem, 1999, 274(51): 36293-36299.
[8]	Santos FR, Diamond-Stanic MK, Prasannarong M, et al. Contribution of the serine kinase c-Jun N-terminal kinase(JNK) to oxidant-induced insulin resistance in isolated rat skeletal muscle [J]. Arch Physiol Biochem, 2012, 118(5): 231-236.
[9]	Skurk T, van Harmelen V, Hauner H, et al. Angiotensin II stimulates the release of interleukin-6 and interleukin-8 from cultured human adipocytes by activation of NF-kappaB [J]. Arterioscler Thromb Vasc Biol, 2004, 24(7): 1199-1203.
[10]	Asamizu S, Urakaze M, Kobashi C, et, al. Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-{alpha} from 3T3-L1 preadipocytes [J]. J Endocrinol, 2009, 202(2): 199-205.
[11]	Lee MH, Song HK, Ko GJ, et, al. Angiotensin receptor blockers improve insulin resistance in type 2 diabetic rats by modulating adipose tissue [J]. Kidney Int, 2008, 74(7): 890-900.
[12]	Tikellis, Wookey PJ, Candido R, et, al. Improved islet morphology after blockade of the renin- angiotensin system in the ZDF rat [J]. Diabetes, 2004, 53(4): 989-997.
[13]	Leung PS, Carlsson PO. Pancreatic islet renin angiotensin system: its novel roles in islet function and in diabetes mellitus [J]. Pancreas, 2005, 30(4): 293-298.
[14]	Darimont, G. Vassaux, G. Ailhaud, et, al. Differentiation of preadipose cells: paracrine role of prostacyclin upon stimulation of adipose cells by angiotensin-Ⅱ [J]. Endocrinology, 1994, 135(5): 2030-2036.
[15]	Fuentes P, Acuna MJ, Cifuentes M, et al. The anti-adipogenic effect of angiotensin II on human preadipose cells involves ERK1, 2 activation and PPARG phosphorylation [J]. J Endocrinol, 2010, 206(1): 75-83.
[16]	Mazak, Fiebeler A, Muller DN, et al. Aldosterone potentiates angiotensin Ⅱ-induced signaling in vascular smooth muscle cells [J]. Circulation, 2004, 109(22): 2792-2800.
[17]	Ishizawa, Izawa Y, Ito H, et, al. Aldosterone stimulates vascular smooth muscle cell proliferation via big mitogen-activated protein kinase 1 activation [J]. Hypertension, 2005, 46(4): 1046-1052.
[18]	Fu GX, Xu CC, Zhong Y, et, al. Aldosterone-induced osteopontin expression in vascular smooth muscle cells involves MR, ERK, and p38 MAPK [J]. Endocrine, 2012, 42(3): 676-683.
[19]	Miyata K, Hitomi H, Guo P, et, al. Possible involvement of Rho-kinase in aldosterone-induced vascular smooth muscle cell remodeling [J]. Hypertens Res, 2008, 31(7): 1407-1413.

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