Author(s): Sharma AM, Chetty VT
Being overweight or obese has become highly prevalent in Western countries and are rapidly reaching epidemic proportions in the developing world. Obesity-related disorders, such as hypertension and diabetes, are also increasing at an alarming rate. The relationship between obesity, hypertension and insulin resistance is well recognised, but the molecular mechanisms involved remain relatively poorly understood. Adipose tissue plays a key role in the pathogenesis of the metabolic syndrome. It serves as an important source of pro-inflammatory molecules, including leptin, tumour necrosis factor alpha, angiotensin II and interleukin-6, as well as anti-inflammatory molecules, such as adiponectin. Knowledge of how these adipose tissue-derived factors influence metabolic and cardiovascular disease has recently expanded. Leptin is now considered to play a key role in the elevation of sympathetic activity commonly found in obese, hypertensive patients, and decreased secretion of adiponectin appears to be an important predictor of diabetes. The ectopic storage of excess fat in skeletal muscle, liver or pancreas, due to the decreased capacity of adipose tissue to scavenge excess calories, may also play a role in the development of insulin resistance and type 2 diabetes. Overall, continuing research into the relationship between adipose-tissue biology and metabolic abnormalities may lead to a better understanding of the molecular mechanisms underlying the relationship between obesity and cardiovascular disease, and ultimately provide alternative treatments for the control of potentially life-threatening conditions.
Referred From: https://www.ncbi.nlm.nih.gov/pubmed/15868117
Author(s): Arner P
Author(s): Chen MP, Chung FM, Chang DM, Tsai JC, Huang HF, et al.
Author(s): Fantuzzi G
Author(s): Filippatos TD, Randeva HS, Derdemezis CS, Elisaf MS, Mikhailidis DP
Author(s): Adeghate E
Author(s): Alberti KG, Zimmet PZ
Author(s): Laakso M, Pyorala K
Author(s): Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, et al.
Author(s): Kim MK, Lee JH, Kim H, Park SJ, Kim SH, et al.
Author(s): Derosa G, Maffioli P, Salvadeo SA, Ferrari I, Gravina A, et al.
Author(s): Sakamoto A, Ishizaka Y, Toda E, Nagai R, Koike K, et al.
Author(s): Guagnano MT, Romano M, Falco A, Nutini M, Marinopiccoli M, et al.
Author(s): Choi KM, Kim JH, Cho GJ, Baik SH, Park HS, et al.
Author(s): Araki S, Dobashi K, Kubo K, Kawagoe R, Yamamoto Y, et al.
Author(s): Kim JH, Kim SH, Im JA, Lee DC
Author(s): Pfutzner A, Hanefeld M, Lübben G, Weber MM, Karagiannis E, et al.
Author(s): Kaminska A, Kopczynska E, Bronisz A, Zmudzinska M, Bielinski M, et al.
Author(s): Haider DG, Schindler K, Schaller G, Prager G, Wolzt M, et al.
Author(s): García-Fuentes E, García-Almeida JM, García-Arnés J, García-Serrano S, Rivas-Marín J, et al.
Author(s): Chang YH, Chang DM, Lin KC, Shin SJ, Lee YJ
Author(s): Pagano C, Pilon C, Olivieri M, Mason P, Fabris R, et al.
Author(s): Jian WX, Luo TH, Gu YY, Zhang HL, Zheng S et al.
Author(s): López-Bermejo A, Chico-Julià B, Fernàndez-Balsells M, Recasens M, Esteve E, et al.
Author(s): Kershaw EE, Flier JS
Author(s): Fasshauer M, Paschke R