Inflammation: the link between insulin resistance, obesity and diabetes

被引:1648
作者
Dandona, P
Aljada, A
Bandyopadhyay, A
机构
[1] SUNY Coll Buffalo, Div Endocrinol Diabet & Metab, Buffalo, NY 14209 USA
[2] Kaleida Hlth, Buffalo, NY 14209 USA
关键词
D O I
10.1016/j.it.2003.10.013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interieukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
引用
收藏
页码:4 / 7
页数:4
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共 41 条
[1]   Insulin inhibits the pro-inflammatory transcription factor early growth response gene-1 (Egr)-1 expression in mononuclear cells (MNC) and reduces plasma tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) concentrations [J].
Aljada, A ;
Ghanim, H ;
Mohanty, P ;
Kapur, N ;
Dandona, P .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (03) :1419-1422
[2]   Tumor necrosis factor-α inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells [J].
Aljada, A ;
Ghanim, H ;
Assian, E ;
Dandona, P .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2002, 51 (04) :487-491
[3]   The relation of markers of inflammation to the development of glucose disorders in the elderly - The cardiovascular health study [J].
Barzilay, JI ;
Abraham, L ;
Heckbert, SR ;
Cushman, M ;
Kuller, LH ;
Resnick, HE ;
Tracy, RP .
DIABETES, 2001, 50 (10) :2384-2389
[4]   ELEVATED SERUM SIALIC-ACID CONCENTRATION IN NIDDM AND ITS RELATIONSHIP TO BLOOD-PRESSURE AND RETINOPATHY [J].
CROOK, MA ;
TUTT, P ;
PICKUP, JC .
DIABETES CARE, 1993, 16 (01) :57-60
[5]   Insulin inhibits intranuclear nuclear factor κB and stimulates IκB in mononuclear cells in obese subjects:: Evidence for an anti-inflammatory effect? [J].
Dandona, P ;
Aljada, A ;
Mohanty, P ;
Ghanim, H ;
Hamouda, W ;
Assian, E ;
Ahmad, S .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (07) :3257-3265
[6]   Tumor necrosis factor-α in sera of obese patients:: Fall with weight loss [J].
Dandona, P ;
Weinstock, R ;
Thusu, K ;
Abdel-Rahman, E ;
Aljada, A ;
Wadden, T .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (08) :2907-2910
[7]   The anti-inflammatory and potential anti-atherogenic effect of insulin: a new paradigm [J].
Dandona, P ;
Aljada, A ;
Mohanty, P .
DIABETOLOGIA, 2002, 45 (06) :924-930
[8]   The suppressive effect of dietary restriction and weight loss in the obese on the generation of reactive oxygen species by leukocytes, lipid peroxidation, and protein carbonylation [J].
Dandona, P ;
Mohanty, P ;
Ghanim, H ;
Aljada, A ;
Browne, R ;
Hamouda, W ;
Prabhala, A ;
Afzal, A ;
Garg, R .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (01) :355-362
[9]   Low-grade systemic inflammation and the development of type 2 diabetes - The atherosclerosis risk in communities study [J].
Duncan, BB ;
Schmidt, MI ;
Pankow, JS ;
Ballantyne, CM ;
Couper, D ;
Vigo, A ;
Hoogeveen, R ;
Folsom, AR ;
Heiss, G .
DIABETES, 2003, 52 (07) :1799-1805
[10]   Fibrinogen, other putative markers of inflammation, and weight gain in middle-aged adults - The ARIC study [J].
Duncan, BB ;
Schmidt, MI ;
Chambless, LE ;
Folsom, AR ;
Carpenter, M ;
Heiss, G .
OBESITY RESEARCH, 2000, 8 (04) :279-286