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Resistin in Rodents and Humans
Hyeong Kyu Park, Rexford S. Ahima
Diabetes Metab J. 2013;37(6):404-414.   Published online December 12, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.6.404
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AbstractAbstract PDFPubReader   

Obesity is characterized by excess accumulation of lipids in adipose tissue and other organs, and chronic inflammation associated with insulin resistance and an increased risk of type 2 diabetes. Obesity, type 2 diabetes, and cardiovascular diseases are major health concerns. Resistin was first discovered as an adipose-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents. Adipocyte-derived resistin is increased in obese rodents and strongly related to insulin resistance. However, in contrast to rodents, resistin is expressed and secreted from macrophages in humans and is increased in inflammatory conditions. Some studies have also suggested an association between increased resistin levels and insulin resistance, diabetes and cardiovascular disease. Genetic studies have provided additional evidence for a role of resistin in insulin resistance and inflammation. Resistin appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and formation of foam cells. Indeed, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with coronary artery disease and ischemic stroke. There is also growing evidence that elevated resistin is associated with the development of heart failure. This review will focus on the biology of resistin in rodents and humans, and evidence linking resistin with type 2 diabetes, atherosclerosis, and cardiovascular disease.

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Original Articles
Adipokine Concentrations in Pregnant Korean Women with Normal Glucose Tolerance and Gestational Diabetes Mellitus.
Eun Suk Oh, Jung Hee Han, Sung Min Han, Jee Aee Im, Eun Jung Rhee, Cheol Young Park, Ki Won Oh, Won Young Lee
Korean Diabetes J. 2009;33(4):279-288.   Published online August 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.4.279
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  • 25 Download
  • 3 Crossref
AbstractAbstract PDF
BACKGROUND
The aims of this study were to compare adipokine concentrations of pregnant women in the 24th~28th weeks of gestation to those of non-pregnant women. We compared the concentrations of adipokines in women with gestational diabetes mellitus (GDM), gestational impaired glucose tolerance (GIGT) and normal glucose tolerance (NGT). We also investigated the role of adipokines in the development of gestational glucose intolerance. METHODS: We surveyed 129 pregnant women who underwent a 100 g oral glucose tolerance test (OGTT) during the 24th~28th weeks of gestation. Participants were classified into three groups: (1) NGT (n = 40), (2) GIGT (n = 45), and (3) GDM (n = 44). Pregnant subjects with NGT were matched to non-pregnant controls for BMI and age (n = 41). RESULTS: Pregnant women with NGT exhibited significantly decreased adiponectin levels and elevated leptin levels compared to non-pregnant controls. Mean plasma resistin levels were significantly higher in women with GDM and GIGT than in women with NGT. Resistin and fasting glucose were significant predictors for the development of gestational glucose intolerance. CONCLUSION: Plasma adiponectin levels were decreased and leptin levels were increased in pregnant subjects with NGT compared to BMI and age matched non-pregnant controls. Women with GDM and GIGT exhibit significantly elevated concentrations of resistin compared with women with NGT. Increased resistin levels were also associated with the development of gestational glucose intolerance. Resistin may play an important role on the development of gestational glucose intolerance in Korean women.

Citations

Citations to this article as recorded by  
  • Maternal serum level of resistin is associated with risk for gestational diabetes mellitus: A meta-analysis
    Shi-Min Hu, Meng-Shi Chen, Hong-Zhuan Tan
    World Journal of Clinical Cases.2019; 7(5): 585.     CrossRef
  • Letter: Adipokines and Insulin Resistance According to Characteristics of Pregnant Women with Gestational Diabetes Mellitus (Diabetes Metab J 2017;41:457-65)
    Ohk-Hyun Ryu
    Diabetes & Metabolism Journal.2018; 42(1): 87.     CrossRef
  • Adipokines and Insulin Resistance According to Characteristics of Pregnant Women with Gestational Diabetes Mellitus
    Eon Ju Jeon, Seong Yeon Hong, Ji Hyun Lee
    Diabetes & Metabolism Journal.2017; 41(6): 457.     CrossRef
Common Genetic Polymorphisms in the Promoter of Resistin Gene are Major Determinants of Plasma Resistin Concentrations in Humans.
Young Min Cho, Byung Soo Youn, Sung Soo Chung, Ki Woo Kim, Bo Kyeong Koo, Kang Yeol Yu, Hong Je Park, Hyoung Doo Shin, Hak Chul Jang, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2004;28(1):9-19.   Published online February 1, 2004
  • 1,238 View
  • 23 Download
AbstractAbstract PDF
BACKGROUND
Resistin has been postulated to be an important link between obesity and insulin resistance. Genetic polymorphisms in the resistin gene promotor have been suggested as a determinant of the expression of resistin mRNA, which is possibly associated with obesity and insulin resistance. In this study, the association between the genotype of the resistin promoter, and its plasma concentrations, were investigated. METHODS: The g.-537A>C and g.-420C>G polymorphisms in the resistin promoter were examined, and the levels of plasma resistin measured in the Korean subjects, both with and without type 2 diabetes. Haplotype-based promoter activity and the gel electrophoretic mobility-shift assays(EMSA) were also performed. RESULTS: The -420G and the -537A alleles, which were in linkage disequilibrium, were associated with higher plasma resistin concentrations. Individuals with the A-G(-537 A and -420G) haplotypes showed significantly higher plasma resistin levels than those that did not. The haplotypes A-G had modestly increased promoter activities compared to the other haplotypes. The EMSA revealed the -420 G allele to be specific for binding of the nuclear proteins from adipocytes and monocytes. However, neither polymorphism was associated with type 2 diabetes or obesity in our study subjects. CONCLUSION: Polymorphisms in the promoter of the resistin gene are major determinants of plasma resistin concentrations in humans
Randomized Controlled Trial
The Effects of Insulin Sensitizers on the Plasma Concentrations of Adipokines in Type 2 Diabetic Patients.
Hye Seung Jung, Young Min Cho, Kyung Won Kim, Byung Soo Youn, Kang Yeol Yu, Hong Je Park, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee, Kyong Soo Park
Korean Diabetes J. 2003;27(6):476-489.   Published online December 1, 2003
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AbstractAbstract PDF
BACKGROUND
Resistin, leptin and adiponectin are proteins secreted from adipose tissue, and have been suggested to play roles in insulin sensitivity. The effects of the circulating levels of two different types of insulin sensitizer, rosiglitazone and metformin, in type 2 diabetic patients were examined to elucidate the relationship between adipokines and insulin resistance. METHODS: Thirty type 2 diabetic patients, who showed poor glycemic control when administered 4 mg glimepiride a day, without severe diabetic complications or medical illness, were randomized to receive an additional 4mg rosiglitazone or 1000 mg metformin a day. The plasma resistin, leptin and adiponectin concentrations were measured at the baseline and after 6 months of treatment. The anthropometric parameters, fasting plasma glucose, HbA1C, total cholesterol, triglyceride, HDL-cholesterol and free fatty acids were also measured. Certain single nucleotide polymorphisms of adipokine genes were also identified. RESULTS: There were no significant differences in the reductions of the plasma glucose and HbA1C levels, after 6 months of treatment, between the two groups. The plasma resistin concentrations decreased, the adiponectin significantly increased and the leptin showed a tendency to increase in the rosiglitazone group. In the metformin group, only the resistin concentration significantly increased. However, the changes in the adipokines did not correlate with the HOMA-IR in either group. The reduction in the HbA1C due to rosiglitazone was greater if the initial leptin level was high, if there was a G allele on the -420th locus of the resistin gene, or the 45th locus of the APM1 (adiponectin gene) was the T-homozygote or there was a T allele on the 276th locus of the APM1. Those due to metfromin were greater with high initial adiponectin levels. CONCLUSION: In type 2 diabetic patients, showing poor glycemic control with sulfonylurea therapy, rosiglitazone or metformin treatment changed some of the adipokine concentrations, but these changes were not clearly related with insulin resistance. Polymorphisms of certain adipokine genes seem to have a relation to the susceptibility of rosiglitazone.

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