Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity

Arita, Yukio; Kihara, Shinji; Ouchi, Noriyuki; Takahashi, Masahiko; Maeda, Kazuhisa; Miyagawa, Jun‐ichiro; Hotta, Kikuko; Shimomura, Iichiro; Nakamura, Tadashi; Miyaoka, Koji; Kuriyama, Hiroshi; Nishida, Makoto; Yamashita, Shizuya; Okubo, Kosaku; Mitsudo, Kenji; Muraguchi, Masahiro; Ohmoto, Yasuichi; Funahashi, Tohru; Matsuzawa, Yūji

doi:10.1006/bbrc.1999.0255

Cited by 4,305 publications

(3,469 citation statements)

References 9 publications

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“…Plasma levels of adiponectin decrease in obese humans [6]. In our study, however, the induction of adiponectin by EPA/DHA could not result from reduction of adiposity, Transcript levels were evaluated by qRT-PCR using RNA isolated from whole tissues or collagenase-liberated adipocytes.…”

Section: Discussionmentioning

confidence: 59%

Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

et al. 2006

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Aims/hypothesis: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin. Methods: We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated. Results: In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA. Conclusions/interpretation: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects.

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Section: Discussionmentioning

confidence: 59%

Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

et al. 2006

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“…[12][13][14][15][16] Adiponectin is the most abundant fat-specific hormone, being exclusively expressed by and secreted from adipose tissue. 17 The plasma adiponectin concentration is decreased in obese individuals 17,18 and patients with type 2 diabetes, 19 and its level is closely related to whole-body insulin sensitivity. 20 This protein is abundant in the circulation 18 and suppresses attachment of monocytes to endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…17 The plasma adiponectin concentration is decreased in obese individuals 17,18 and patients with type 2 diabetes, 19 and its level is closely related to whole-body insulin sensitivity. 20 This protein is abundant in the circulation 18 and suppresses attachment of monocytes to endothelial cells. 21 Adiponectin also stimulates the production of nitric oxide (NO) by vascular endothelial cells, resulting in the improvement of endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Effect of nifedipine on adiponectin in hypertensive patients with type 2 diabetes mellitus

et al. 2006

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Nifedipine, a dihydropyridine calcium antagonist, improves endothelial function in patients with hypercholesterolaemia by enhancing nitric oxide (NO) activity, and increases endothelial NO bioavailability by antioxidant mechanisms. We administered a long-acting nifedipine formulation (controlled release (CR) nifedipine: 20 mg/day) to hypertensive patients for 6 months. There were no other changes of drug treatment during therapy with CR nifedipine. Clinical and biochemical data obtained before and after CR nifedipine administration were compared. All markers were measured by enzyme-linked immunosorbant assay. The levels of soluble markers (soluble CD40 ligand, soluble P-selectin, and soluble E-selectin), microparticles (MP) (platelet-derived MP, monocyte-derived MP, and endothelial cell-derived MP), and adiponectin differed between the control group and the hypertension group. The levels of these markers were also different in hypertensive patients with and without type 2 diabetes compared with the control group. In the hypertensive patients with type 2 diabetes, all markers except adiponectin decreased significantly after 3 months of CR nifedipine treatment. In contrast, markers were unchanged in the hypertensive patients without type 2 diabetes. Adiponectin was increased after 6 months of CR nifedipine treatment in hypertensive patients with type 2 diabetes. The effects of CR nifedipine on platelet/monocyte activation and adiponectin levels demonstrated in the present study indicate the potential effectiveness of calcium antagonist therapy for hypertensive patients with type 2 diabetes.

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“…This means that obesity is shown to be independent risk factor for GERD and is correlated with severity. Several clinical studies showed decreased adiponectin levels in obese humans relative to lean subjects such as studies by Arita et al 7. and Hotta et al 25.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, adiponectin is an adipocytokine that was isolated from the human adipose tissue. It ranges from 5 to 30 μg/mL in the human blood, and serum levels are inversely correlated with body mass index (BMI) 7. Moreover, adiponectin has anti‐inflammatory, anti‐steatotic, anti‐diabetic, and anti‐malignant effects.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin level changes among Egyptians with gastroesophageal reflux disease

et al. 2018

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Background and AimVisceral fat is an important endocrine organ that secretes different bioactive substances such as adipocytokines. The aim of this study was to investigate the adiponectin level changes among patients with erosive gastroesophageal reflux disease (GERD)and its consequence on pathogenesis.MethodsIn this study, 150 subjects were selected and divided into four groups: Group І (n = 40) were healthy individuals with an average body mass index and had no gastrointestinal tract symptoms; Group ІІ (n = 50) were patients with mild to moderate erosive esophagitis; Group ІІІ (n = 40) were patients with severe erosive esophagitis; and finally, Group ІV (n = 20) were patients with Barrett's esophagus. Upper gastrointestinal endoscopy was performed for Groups II, III, and IV only, and histopathological assessment was conducted for the suspicious cases of Barrett's esophagus. The measurement of serum adiponectin was performed for all groups using the ELISA test.ResultsOur results revealed that the serum level of adiponectin was significantly lower in patients with different grades of GERD as well Barrett's esophagus as compared to healthy controls (P‐value < 0.001). Additionally, the serum level of adiponectin was correlated with different grades of GERD as the highest level of the adiponectin was found in the control group (11.05 ± 2.58) followed by mild to moderate GERD (6.39 ± 1.64) and then severe GERD (2.42 ± 1.00); finally, the lowest level was detected in the Barrett's esophagus group (1.99 ± 0.47). Our study showed significant correlation between body mass index, waist circumference, and waist–hip ratio on one hand and serum adiponectin level on the other hand, with a statistically significant difference (P‐value < 0.001). The best cut‐off value for serum adiponectin was 7.7 (μg/mL), with a sensitivity of 91.8% and specificity of 97.5%.ConclusionsLow serum adiponectin level appears to be associated with an increased risk of erosive esophagitis, and visceral fat accumulation is related to the impaired secretion of adiponectin, which may have an influence on the pathogenesis of GERD.

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Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity

Cited by 4,305 publications

References 9 publications

Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

Effect of nifedipine on adiponectin in hypertensive patients with type 2 diabetes mellitus

Adiponectin level changes among Egyptians with gastroesophageal reflux disease

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