Resistin May Be Biochemical Link Between Obesity And Type 2 Diabetes

Main Category: Obesity / Weight Loss / Fitness
Also Included In: Diabetes;  Biology / Biochemistry
Article Date: 17 Jan 2008 - 5:00 PDT

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Obesity is a worldwide health problem directly linked to several diseases such as hypertension and type 2 diabetes. Resistin is a cysteine-rich hormone mainly secreted by adipose tissues and may form a biochemical link between obesity and type 2 diabetes.

It has been reported insulin inhibits resistin mRNA level in 3T3-L1, which does not support a role for resistin in insulin resistance. Does resistin play a role in insulin resistance? Is insulin the major regulator of resistin?

A research article published on January 7, 2008 in the World Journal of Gastroenterology (volume 14, issue 1) addresses these questions. The research team led by Dr. Guo Xi-Rong studied the resistin action in vitro and resistin secretion. In addition to this, diet-induced obese rats were used to study the relationship between insulin, resistin and insulin resistance.

One result reported by the investigators was resistin expression and secretion was enhanced during 3T3-L1 pre-adipocytes differentiation, insulin inhibits resistin expression and secretion. Insulin does not support a role for resistin in insulin resistance.

The result showed resistin induces cellular insulin resistance in H4IIE hepatocytes and L6 rat myoblasts. Serum resistin negatively correlates to insulin sensitivity, not to serum insulin in diet-induced obesity rats.

The results of this study suggest insulin inhibits resistin secretion and resistin induces insulin sensitivity. In vivo study shows serum resistin correlated to rat insulin sensitivity, so insulin is not the major regulator of resistin. Resistin induced hepatocytes insulin resistance takes part in diet induced insulin resistance.

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6.1 Reference: Liu F, Fan HQ, Qiu J, Wang B, Zhang M, Gu N, Zhang CM, Fei L, Pan XQ, Guo M, Chen RH, Guo XR. A paradox: Insulin inhibits expression and secretion of resistin which induces insulin resistance. World J Gastroenterol 2008; 14(1): 95-100 http://www.wjgnet.com/1007-9327/14/95.asp

6.2 Correspondence to: Department of Pediatrics, Nanjing Maternity and Child Health Hospital, Nanjing Medical University, Nanjing, 210004, China.

6.3 About World Journal of Gastroenterology

World Journal of Gastroenterology
(WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. The WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

6.4 About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Source: Jing Zhu
World Journal of Gastroenterology

Article adapted by Medical News Today from original press release.
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Jing Zhu. "Resistin May Be Biochemical Link Between Obesity And Type 2 Diabetes." Medical News Today. MediLexicon, Intl., 17 Jan. 2008. Web.
13 Feb. 2012. <http://www.medicalnewstoday.com/releases/94305.php>

APA
Jing Zhu. (2008, January 17). "Resistin May Be Biochemical Link Between Obesity And Type 2 Diabetes." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/94305.php.

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