Effects of pioglitazone on metabolic parameters, body fat distribution, and serum adiponectin levels in Japanese male patients with type 2 diabetes

Hara, Hiroshi; Kawai, Takeshi; Yamamoto, Yukihiro; Taniyama, Matsuo; Tomita, Motowo; Matsubara, Koichi; Okazaki, Yoshiaki; Ishii, Tatsuya; Oguma, Yuko; Takei, Izumi; Saruta, Takao

doi:10.1053/meta.2002.30506

Cited by 223 publications

(132 citation statements)

References 29 publications

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“…Drug treatment for hypertension was found to significantly increase both adiponectin and IS, 31 as did the use of insulin sensitizing drugs. 32 Similar outcomes were also observed for dietary modulations. 33,34 Overall, adiponectin may have a role in the pathogenesis of the syndrome via insulin-sensitizing effects.…”

Section: Does Adiponectin Have a Role?supporting

confidence: 62%

Factors determining the risk of the metabolic syndrome: is there a central role for adiponectin?

2013

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EK Calton, VS Miller and MJ SoaresBACKGROUND AND OBJECTIVES: The pathogenesis of the metabolic syndrome (MetS) is not well understood. This review is based on the hypothesis that both traditional and emerging risk factors act through adiponectin. SUBJECTS AND METHODS:We conducted a search of the literature using prominent electronic databases and search terms that included in combination: adiponectin, diet, dietary patterns, exercise, metabolic rate, MetS and testosterone. Articles were restricted to studies conducted on adult humans, reported in English and within the time period 2000-2012. RESULTS AND CONCLUSIONS: Both traditional and emerging risk factors associated with the MetS show some evidence of exerting their influence through adiponectin. High-quality randomized controlled trials that alter adiponectin levels are required to further corroborate this hypothesis. INTRODUCTIONThe metabolic syndrome (MetS) represents a clustering of risk factors for cardiovascular disease and type 2 diabetes mellitus (T2DM), which include: hypertension, low high-density lipoproteincholesterol (HDL-C), high triglycerides (TG), high fasting blood glucose (FBG) and abdominal obesity. 1 Obesity and insulin resistance (IR) have long been accepted as having a pivotal role in the etiopathogenesis of the syndrome. 2,3 However, emerging evidence indicates that even after controlling for these variables, there remains a substantial unexplained risk. 2,[4][5][6] Adiponectin, a collagen-like protein was first discovered in 1995 by Dcherer and Lodish, who called it adipocyte complementrelated protein of 30 kDa (Acrp30). 7 At a similar time, three other independent groups discovered adiponectin, calling it adipose most abundant gene transcript 1 (apM1), AdipoQ and gelatinbinding protein of 28 kDa (GBP28). 8 Adiponectin is secreted primarily from adipose tissue into the circulation where highmolecular-weight, medium-molecular-weight and low-molecularweight oligomeric forms exist. 8,9 Total adiponectin as well as the individual oligomeric forms have been associated with health benefits. 9 Consistent links between low adiponectin levels and increased TG, FBG, waist circumference, blood pressure (BP) levels and decreased HDL-C explain its potential role in the etiology of MetS. 2,10 Furthermore, genetic studies have linked adiponectin and MetS in individuals of European descent. 11 Specifically, overall adiposity, abdominal adiposity and IR were influenced by gene loci, which also encode adiponectin. 12 This review discusses both traditional and emerging factors that may influence the prevalence of MetS. Furthermore, the possibility that adiponectin may have an important role in the pathogenesis of the syndrome was evaluated. As there is inconsistency in the literature whether total, high-molecular-weight, mediummolecular-weight or low-molecular-weight adiponectin was measured, 4,13,14 this review discusses adiponectin in general terms. We present a model that emphasizes the flow-through effects of several factors on MetS risk through adi...

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Section: Does Adiponectin Have a Role?supporting

confidence: 62%

Factors determining the risk of the metabolic syndrome: is there a central role for adiponectin?

2013

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“…[4][5][6][7] PIO increases adipocyte differentiation and stimulates the distribution of new adipose tissue to both retroperitoneal and subcutaneous sites by activation of PPARγ receptors. 4 Most studies show that PIO have an overall beneficial effect since PIO was found to increase HDL-C and lowered plasma TG and VLDL.…”

Section: Discussionmentioning

confidence: 99%

“…4 In past studies, PIO has inconsistent effects on lipid profile parameters. [4][5][6][7] The objective of the present study was, therefore, to investigate exact effect of PIO on different lipid profile parameters and also its antioxidant effect in hyperlipidemic rats.…”

Section: Introductionmentioning

confidence: 99%

Hypolipidemic and antioxidant activities of pioglitazone in hyperlipidemic rats

Bhosale

Jadhav

Padwal

et al. 2013

Int J Basic Clin Pharmacol

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Background: Diabetes mellitus (DM) is an endocrine disorder characterized by abnormal carbohydrate, lipid and protein metabolism along with specific long-term complications which are associated with hyperlipidemia and oxidative stress. Hence, it is important to find hypoglycemic drug that improves lipid profile and reduces oxidative stress in diabetic patient. This study, therefore, was performed to investigate hypolipidemic and antioxidant potential of Pioglitazone (PIO) in hyperlipidemic rats. Methods: Hyperlipidemia was induced in normal rats by including 0.75 gm% cholesterol and 1.5 gm% bile salt in normal diet and these rats were used for the experiments. PIO hydrochloride was administered as 10 mg/kg and 30 mg/kg dose levels to the hyperlipidemic rats. Hypolipidemic activity was estimated by plasma lipid profile parameters while antioxidant potential was estimated by ascorbic acid, catalase activity, malondialdehyde and superoxide dismutase activity using standard methods. Statistical analysis was done by one way analysis of variance (ANOVA) followed by Dunnett’s test. Results: Treatment with 10 mg/kg and 30 mg/kg dose levels of PIO hydrochloride resulted in a significant decrease in serum TG and VLDL only in 30 mg/kg PIO treated group and significant increase in serum HDL in both groups, but no significant decrease in cholesterol and LDL in both PIO treated groups. PIO increased activities of catalase enzyme and concentration of malondialdehyde significantly in only 30 mg/kg PIO treated group. But there were no significant changes in the superoxide dismutase activity and ascorbic acid concentration in both PIO treated groups. Conclusions: The present study demonstrated that treatment with 10 mg/kg and 30 mg/kg dose levels of PIO hydrochloride improves the plasma lipid profile and also reduces oxidative stress in hyperlipidemic animals. [Int J Basic Clin Pharmacol 2013; 2(1.000): 77-82

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“…Serum adiponectin levels are known to be reduced in both childhood and adult obesity [1,2]. Decreased serum adiponectin can serve as a potent predictor of the future development of insulin resistance, type 2 diabetes and cardiovascular disease [3,4]. In addition, the human adiponectin gene has been mapped to locus 3q27, which has been identified as a susceptibility locus for type 2 diabetes and the metabolic syndrome [5].…”

Section: Introductionmentioning

confidence: 99%

Serum high molecular weight complex of adiponectin correlates better with glucose tolerance than total serum adiponectin in Indo-Asian males

et al. 2005

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Aims/hypothesis: It is well established that total systemic adiponectin is reduced in type 2 diabetic subjects. To date most studies have been concerned with the singular full-length protein or proteolytically cleaved globular domain. It is, however, apparent that the native protein circulates in serum as a lower molecular weight hexamer and as larger multimeric structures of high molecular weight (HMW). In this study we address the clinical significance of each form of the protein with respect to glucose tolerance. Methods: Serum was obtained from 34 Indo-Asian male subjects (BMI 26.5±3.1; age 52.15±10.14 years) who had undertaken a 2-h oral glucose tolerance test. An aliquot of serum was fractionated using velocity sedimentation followed by reducing SDS-PAGE. Western blots were probed for adiponectin, and HMW adiponectin as a percentage of total adiponectin (percentage of higher molecular weight adiponectin [S A ] index) was calculated from densitometry readings. Total adiponectin was measured using ELISA; leptin, insulin and IL-6 were determined using ELISA. Results: Analysis of the cohort demonstrated that total adiponectin (r=0.625, p=0.0001), fasting insulin (r=−0.354, p=0.040) and age (r=0.567, p=0.0001) correlated with S A . S A showed a tighter, inverse correlation with 2-h glucose levels (r=−0.58, p=0.0003) than total adiponectin (r=−0.38, p=0.0001). Conclusions/interpretation: This study demonstrates the importance of the S A index as a better determinant of glucose intolerance than measurements of total adiponectin. Our findings suggest that HMW adiponectin is the active form of the protein.

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Effects of pioglitazone on metabolic parameters, body fat distribution, and serum adiponectin levels in Japanese male patients with type 2 diabetes

Cited by 223 publications

References 29 publications

Factors determining the risk of the metabolic syndrome: is there a central role for adiponectin?

Factors determining the risk of the metabolic syndrome: is there a central role for adiponectin?

Hypolipidemic and antioxidant activities of pioglitazone in hyperlipidemic rats

Serum high molecular weight complex of adiponectin correlates better with glucose tolerance than total serum adiponectin in Indo-Asian males

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