Plasma Resistin Concentrations Measured by Enzyme-Linked Immunosorbent Assay Using a Newly Developed Monoclonal Antibody Are Elevated in Individuals with Type 2 Diabetes Mellitus

Youn, Byung-Soo; Yu, Kang-Yeol; Park, Hong Je; Lee, Nam Seok; Min, Sung Shik; Youn, Moon Yeon; Cho, Young Min; Park, Young Joo; Kim, Seong Yeon; Lee, Hong Kyu; Park, Kyong Soo

doi:10.1210/jc.2003-031121

Cited by 190 publications

(139 citation statements)

References 29 publications

(39 reference statements)

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“…Although data suggest that resistin levels are elevated in subjects with type 2 diabetes mellitus, 22 previous data in reference to resistin and NAFLD are conflicting. Resistin levels have been shown to be higher in patients with high grade steatosis compared with low grade steatosis 23 and are related to the histopathologic severity of disease.…”

Section: Discussionmentioning

confidence: 93%

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Fecht²,

et al. 2008

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The aim of this study was to determine if orlistat, an inhibitor of fat absorption, combined with caloric restriction in overweight subjects with nonalcoholic steatohepatitis results in weight loss and improved liver histology. Fifty overweight subjects (body mass index ‫؍‬ >27) with biopsy proven nonalcoholic steatohepatitis were randomized to receive a 1,400 Kcal/day diet plus vitamin E (800 IU) daily with or without orlistat (120 mg three times a day) for 36 weeks. Liver biopsies were repeated at week 36. Twenty-three subjects in the orlistat/diet/vitamin E group and 18 in the diet/vitamin E group completed the study. The mean age was 47 ؎ 9.0 (standard deviation) years and mean body mass index was 36.4 ؎ 6.3 kg/m 2 . Four subjects were diabetic. The orlistat group lost a mean of 8.3% body weight compared to 6.0% in the diet plus vitamin E group (not significant). Both groups also had similarly improved serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty liver disease activity scores. Stratified according to weight loss instead of treatment group, a loss of >5% body weight (n ‫؍‬ 24) compared to <5% body weight (n ‫؍‬ 17) correlated with improvement in insulin sensitivity (P ‫؍‬ 0.001) and steatosis (P ‫؍‬ 0.015). Comparing subjects who lost >9% of body weight (n ‫؍‬ 16), to those that did not (n ‫؍‬ 25), improved insulin sensitivity (P < 0.001), adiponectin (P ‫؍‬ 0.03), steatosis (P ‫؍‬ 0.005), ballooning (P ‫؍‬ 0.04), inflammation (P ‫؍‬ 0.045), and nonalcoholic fatty liver disease activity score (P ‫؍‬ 0.009) were seen. Increases in adiponectin strongly correlated with improved ballooning and nonalcoholic fatty liver disease activity score (P ‫؍‬ 0.03). Orlistat did not enhance weight loss or improve liver enzymes, measures of insulin resistance, and histopathology. However, subjects who lost >5% of body weight over 9 months improved insulin resistance and steatosis, and those subjects who lost >9% also achieved improved hepatic histologic changes. (HEPATOLOGY 2009;49:80-86.)

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Section: Discussionmentioning

confidence: 93%

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Fecht²,

et al. 2008

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“…The major risk factors of type 2 diabetes include obesity and insulin resistance with associated impaired secretion of various adipokines (Youn et al 2004;Weyer et al 2001). A number of molecules involved in inflammatory processes have been investigated for their role in type 2 diabetes (Duncan et al 2003;Schmidt et al 1999;Pradhan et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Association analysis of TNFRSF1B polymorphisms with type 2 diabetes and its related traits in North India

Tabassum

Chavali

Ghosh

et al. 2008

HUGO J

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Inflammation plays a crucial role in the pathogenesis of type 2 diabetes and various lines of evidences suggest an important contribution of type 2 receptor for TNFa (TNFR2), a mediator of inflammatory responses. Though genetic association of TNFRSF1B (encoding TNFR2) polymorphisms have been investigated in various studies, their involvement is not clear because of inconsistent findings. Because of high susceptibility of Indian population to type 2 diabetes and its complications, we evaluated the association of TNFRSF1B polymorphismsrs1061622 (M196R; exon6) and rs3397 (3 0 UTR) and (CA) n repeat (intron 4) in 1,852 subjects including 1,040 cases and 812 controls with type 2 diabetes and its associated peripheral neuropathy and hypertension in North Indians of Indo-European ethnicity. The allelic and genotypic distributions of these polymorphisms were comparable among healthy control vs. type 2 diabetes, peripheral neuropathy vs. non-neuropathy and hypertensive vs. normotensive groups. (CA) n polymorphism has been shown to be associated with diabetic neuropathy in Caucasians, however, this could not be replicated in our study (P = 0.27). None of the polymorphisms were found to influence the 14 anthropometric and biochemical traits related to type 2 diabetes studied here. Thus, we conclude that TNFRSF1B is not a major contributing factor to the genetic risk of type 2 diabetes, its associated peripheral neuropathy and hypertension and related metabolic traits in North Indians.

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“…Three specific DNA-protein complexes (bands 1, 2 and 3) and free probes are indicated. The −420G/C variation-independent band is indicated by an asterisk, and the fact that this band is not related to the −420G/C variation was proven in the previous work [21] of resistin in the media was measured using a mouse resistin ELISA kit according to the manufacturer's instructions (Komed, Seoul, Korea) [11].…”

Section: Methodsmentioning

confidence: 96%

“…Levels of resistin expression are similar in normal, insulin-resistant and type 2 diabetic individuals [9]. Recently, however, we observed that plasma resistin levels were elevated in patients with type 2 diabetes compared with those in non-diabetic individuals [11]. Moreover, mice lacking the resistin gene show that resistin plays an important role in the maintenance of blood glucose during fasting, by increasing hepatic glucose production [12].…”

Section: Introductionmentioning

confidence: 94%

Regulation of human resistin gene expression in cell systems: an important role of stimulatory protein 1 interaction with a common promoter polymorphic site

et al. 2005

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Aims/hypothesis: Resistin is an adipokine that might link obesity and insulin resistance. A common polymorphism of the human resistin gene, −420C>G, is a major determinant of plasma resistin concentrations as well as resistin mRNA expression in human adipose tissue. In this study, we investigated the regulatory mechanism by which this polymorphism affects resistin expression. Methods: Electrophoretic mobility shift assay was performed to identify the transcription factors binding to the −420G region. Transient transfection and reporter assay were used to measure promoter activities of the resistin gene. The binding ability of stimulatory protein 1 (Sp1) in response to adipocyte differentiation or high glucose concentrations was also measured. Results: Sp1 and stimulatory protein 3 (Sp3) specifically bound to the region around −420G of the human resistin gene. Overexpression of Sp1 increased the promoter activity regardless of −420 genotypes, while the promoter activity of the −420G construct was two-fold higher than that of the −420C construct. In contrast, overexpression of Sp3 scarcely increased the promoter activity. The binding ability of Sp1 to the −420G region was increased in response to adipocyte differentiation. Mithramycin A, an inhibitor of DNA binding of Sp1, reduced the effect of high glucose on transcription induction of the resistin gene in adipocytes. Conclusions/interpretation: These results suggest that Sp1 is an important factor regulating transcription of human resistin gene. A common polymorphism of the human resistin promoter, −420C>G, is critical for the binding of Sp1 and modulates the transcriptional activity of the resistin gene by changing the binding ability of Sp1. In addition, Sp1 may be involved in the increase of resistin expression by hyperglycaemia.

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Plasma Resistin Concentrations Measured by Enzyme-Linked Immunosorbent Assay Using a Newly Developed Monoclonal Antibody Are Elevated in Individuals with Type 2 Diabetes Mellitus

Cited by 190 publications

References 29 publications

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial

Association analysis of TNFRSF1B polymorphisms with type 2 diabetes and its related traits in North India

Regulation of human resistin gene expression in cell systems: an important role of stimulatory protein 1 interaction with a common promoter polymorphic site

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