Contribution of adipocyte-derived factors to beta-cell dysfunction in diabetes

被引:72
作者
Zhao, YF
Feng, DD
Chen, C
机构
[1] Prince Henrys Inst Med Res, Melbourne, Vic 3168, Australia
[2] Fourth Mil Med Univ, Dept Physiol, Xian 710032, Peoples R China
[3] Ctr S Univ, Xiangya Med Sch, Dept Physiol, Changsha, Peoples R China
关键词
adipocyte; type; 2; diabetes; insulin resistance; adiponectin; FFAs; TNF; IL-6;
D O I
10.1016/j.biocel.2005.11.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In addition to serving as an energy reservoir, the adipocyte has been characterized as an endocrine cell, secreting many bioactive factors which influence energy homeostasis. Being overweight, with excessive adipose tissue, is considered to be part of the pathogenesis of type 2 diabetes. Insulin resistance and beta-cell dysfunction are two major pathophysiological changes seen in type 2 diabetes. In addition to inducing insulin resistance in insulin-responsive tissues, adipocyte-derived factors play an important role in the pathogenesis of beta-cell dysfunction. Leptin, free fatty acids, adiponectin, tumor necrosis factor-a and interleukin-6 are all produced and secreted by adipocytes, and may directly influence aspects of beta-cell function, including insulin synthesis and secretion, insulin cell survival and apoptosis. During the progression from normal weight to obesity and on to overt diabetes, the adipocyte-derived factors contribute to the occurrence and development of beta-cell dysfunction and type 2 diabetes. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:804 / 819
页数:16
相关论文
共 158 条
[21]   Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin on insulin secretion [J].
Emilsson, V ;
Liu, YL ;
Cawthorne, MA ;
Morton, NM ;
Davenport, M .
DIABETES, 1997, 46 (02) :313-316
[22]   Adiponectin gene expression and secretion is inhibited by interleukin-6 in 3T3-L1 adipocytes [J].
Fasshauer, M ;
Kralisch, S ;
Klier, M ;
Lossner, U ;
Bluher, M ;
Klein, J ;
Paschke, R .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 301 (04) :1045-1050
[23]   Leptin: A potent inhibitor of insulin secretion [J].
Fehmann, HC ;
Peiser, C ;
Bode, HP ;
Stamm, M ;
Staats, P ;
Hedetoft, C ;
Lang, RE ;
Goke, B .
PEPTIDES, 1997, 18 (08) :1267-1273
[24]   β-cell mass dynamics in Zucker diabetic fatty rats -: Rosiglitazone prevents the rise in net cell death [J].
Finegood, DT ;
McArthur, MD ;
Kojwang, D ;
Thomas, MJ ;
Topp, BG ;
Leonard, T ;
Buckingham, RE .
DIABETES, 2001, 50 (05) :1021-1029
[25]   DYNAMICS OF BETA-CELL MASS IN THE GROWING RAT PANCREAS - ESTIMATION WITH A SIMPLE MATHEMATICAL-MODEL [J].
FINEGOOD, DT ;
SCAGLIA, L ;
BONNERWEIR, S .
DIABETES, 1995, 44 (03) :249-256
[26]   LEPTIN LEVELS REFLECT BODY LIPID-CONTENT IN MICE - EVIDENCE FOR DIET-INDUCED RESISTANCE TO LEPTIN ACTION [J].
FREDERICH, RC ;
HAMANN, A ;
ANDERSON, S ;
LOLLMANN, B ;
LOWELL, BB ;
FLIER, JS .
NATURE MEDICINE, 1995, 1 (12) :1311-1314
[27]   Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: Depot difference and regulation by glucocorticoid [J].
Fried, SK ;
Bunkin, DA ;
Greenberg, AS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (03) :847-850
[28]  
Friedman JM, 1998, NUTR REV, V56, pS38
[29]   Leptin and the regulation of body weight in mammals [J].
Friedman, JM ;
Halaas, JL .
NATURE, 1998, 395 (6704) :763-770
[30]   The adipocyte:: a model for integration of endocrine and metabolic signaling in energy metabolism regulation [J].
Frühbeck, G ;
Gómez-Ambrosi, J ;
Muruzábal, FJ ;
Burrell, MA .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2001, 280 (06) :E827-E847