• Biomolecules & Therapeutics
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• v.22 no.5
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• pp.384-389
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• 2014

Adiponectin, an adipokine predominantly secreted from adipose tissue, exhibits diverse biological responses, including metabolism of glucose and lipid, and apoptosis in cancer cells. Recently, adiponectin has been shown to modulate autophagy as well. While emerging evidence has demonstrated that autophagy plays a role in the modulation of proliferation and apoptosis of cancer cells, the role of autophagy in apoptosis of cancer cell caused by adiponectin has not been explored. In the present study, we demonstrated that globular adiponectin (gAcrp) induces both apoptosis and autophagy in human hepatoma cell line (HepG2 cells) and breast cancer cells (MCF-7), as evidenced by increase in caspase-3 activity, Bax, microtubule-associated protein light chain 3-II (LC3 II) protein levels, and autophagosome formation. Interestingly, gene silencing of LC3B, an autophagy marker, significantly enhanced gAcrp-induced apoptosis in both HepG2 and MCF-7 cell lines, whereas induction of autophagy by rapamycin, an mTOR inhibitor, significantly prevented gAcrp-induced apoptosis in hepatoma cells HepG2. Furthermore, modulation of autophagy produced similar effects on gAcrp-induced Bax expression in HepG2 cells. These results implicate that induction of autophagy plays a regulatory role in adiponectin-induced apoptosis of cancer cells, and thus inhibition of autophagy would be a novel promising target to enhance the efficiency of cancer cell apoptosis by adiponectin.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.8
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• pp.1088-1097
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• 2018

Objective: It is commonly accepted that adiponectin binds to its two receptors to regulate fatty acid metabolism in adipocytes. To better understand their functions in the regulation of intramuscular adipogenesis in goats, we cloned the three genes (adiponectin [AdipoQ], adiponectin receptor 1 [AdipoR1], and AdipoR2) encoding these proteins and detected their mRNA distribution in different tissues. We also determined the role of AdipoQ in the adipogenic differentiation of goat skeletal muscle satellite cells (SMSCs). Methods: SMSCs were isolated using 1 mg/mL Pronase E from the longissimus dorsi muscles of 3-day-old female Nanjiang brown goats. Adipogenic differentiation was induced in satellite cells by transferring the cells to Dulbecco's modified Eagle's medium supplemented with an isobutylmethylxanthine, dexamethasone and insulin cocktail. The pEGFP-N1-AD plasmid was transfected into SMSCs using Lipofectamine 2000. Expression of adiponectin in tissues and SMSCs was detected by quantitative polymerase chain reaction and immunocytochemical staining. Results: The three genes were predominantly expressed in adipose and skeletal muscle tissues. According to fluorescence and immunocytochemical analyses, adiponectin protein expression was only observed in the cytoplasm, suggesting that adiponectin is localized to the cytoplasm of goat SMSCs. In SMSCs overexpressing the AdipoQ gene, adiponectin promoted SMSC differentiation into adipocytes and significantly (p<0.05) up-regulated expression of AdipoR2, acetyl-CoA carboxylase, fatty-acid synthase, and sterol regulatory element-binding protein-1, though expression of CCAAT/enhancer-binding $protein-{\alpha}$, peroxisome proliferator-activated receptor ${\gamma}$, and AdipoR1 did not change significantly. Conclusion: Adiponectin induced SMSC differentiation into adipocytes, indicating that adiponectin may promote intramuscular adipogenesis in goat SMSC.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.10
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• pp.1429-1436
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• 2009

Adiponectin is an adipocyte-derived protein that has a regulatory role in energy homeostasis and influences insulin sensitivity. Its effects on glucose utilization and lipid metabolism are mediated by AdipoR1 and AdipoR2. How insulin affects adiponectin gene expression and secretion is still controversial. This study was conducted to determine the expression of adiponectin, AdipRs and $PPAR-\gamma$ during the differentiation of bovine preadipocytes and the effect of insulin on expression of these genes in bovine adipocytes. The bovine preadipocytes started to accumulate lipids three days after differentiation was induced, with increased expression of adiponectin, AdipoR2 and $PPAR-\gamma$ mRNAs. Insulin decreased the expression of adiponectin mRNA in a dose- and time-dependent fashion, and the inhibition was detectable at insulin concentrations as low as 10 nM and as early as 2 h after addition of 100 nM insulin. Insulin also inhibited the expression of AdipoR2 mRNA at concentrations from 1 to 1,000 nM or 24 h after addition of 100 nM insulin, but did not affect the expression of AdipoR1 in bovine adipocytes. Inhibition of PI3K with LY294002 reversed the inhibition of adiponectin and AdipoR2 mRNA expression by insulin. These results suggest that insulin suppresses the expression of adiponectin and AdipoR2 at least partially via the PI3K signal pathway.

• Annals of dermatology
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• v.30 no.6
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• pp.645-652
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• 2018

Background: Adiponectin, an adipokine secreted from adipocytes, affects energy metabolism and also shows anti-diabetic and anti-inflammatory properties. Recent studies have reported that adiponectin plays a role in regulating skin inflammation. Objective: This study aimed to investigate the effect of adiponectin on the expression of filaggrin (FLG) in normal human epidermal keratinocytes (NHEKs). Methods: NHEKs were serum-starved for 6h before being treated with adiponectin. Afterward, cell viability was assessed by MTT assay. We also treated with calcium, interleukin (IL)-4, and IL-13 to provide positive and negative comparative controls, respectively. Gene mRNA expression was quantified using real time reverse transcription polymerase chain reaction, and protein expression was evaluated using Western blot. To evaluate the relationship among mitogen-activated protein kinases (MAPKs), activator protein 1 (AP-1), and FLG, we also treated cells with inhibitors for MAPKs JNK, p38, and ERK1/2. Results: FLG and FLG-2 mRNA expression in NHEKs significantly increased after treatment with $10{\mu}g/ml$ adiponectin. Adiponectin also restored FLG and FLG-2 mRNA expression that was otherwise inhibited by treatment with IL-4 and IL-13. Adiponectin induced FLG expression via AP-1 and MAPK signaling. Conclusion: Adiponectin positively regulated the expression of FLG and could be useful as a therapeutic agent to control diseases related to disrupted skin barrier function.

• Journal of Life Science
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• v.18 no.11
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• pp.1600-1605
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• 2008

This study was performed to verify the gene expression of 3T3-L1 using the siRNA of the aromatase gene, which is the estrogen synthesis enzymes. First of all three pairs of siRNA were designed from the CYP19A1 (aromatase) and analyzed the formation of fat cell mechanism by transferring gene to 3T3-L1 and differentiating it. As a result, the expression of leptin gene, which is the main gene causing the obesity, was controlled and the cause of the obesity is related with the insulin specifically. The overexpression of adiponectin and adipsin was observed. This result showed that the formation of the fat was controlled a little without any side effect by obstructing a specific material out of all the signal systems in the fat formation. This study will be an important clue to make it clear that the lack or overexpression of estrogen might be the cause of fat formation mechanism.

• BMB Reports
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• v.42 no.10
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• pp.667-672
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• 2009

Plasma concentrations of adiponectin have been shown to be decreased in patients with obesity, cardiovascular diseases, hypertension and metabolic syndrome. Recent studies have found that adiponectin reduces lipid accumulation in macrophage foam cells which may impact the development of atherosclerosis. However, it remains unclear whether adiponectin is involved in the process of lipid accumulation during myogenesis. Using C2C12 myoblasts, we investigated the effect of adiponectin on intramyocellular lipid accumulation during myogenesis. The results showed that intracellular lipid accumulation is significantly decreased during C2C12 differentiation, apparently due to increased fatty acid oxidation and decreased fatty acid synthesis during this process. C2C12 cells transiently transfected with adiponectin gene showed reduced lipid accumulation as compared to controls. Further experiments demonstrated that adiponectin can suppress lipid accumulation by increasing fatty acid oxidation during C2C12 myogenesis.

• Applied Microscopy
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• v.48 no.3
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• pp.62-72
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• 2018

This study investigated the anti-obesity effect of a pear (Fructus Pyri Pyrifoliae) extract fermented by lactic-acid bacteria on obesity induced by a high-fat diet in rats. Body-weight measurement, blood analysis, and light microscope observation of adipose tissue in liver and epididymis were conducted after 8 weeks. Gene expression of leptin, adiponectin, and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) in liver cells were also investigated. Compared to CON, PFA and PFB showed 8% weight reduction along with weight reduction of adipose tissue in liver and epididymis. Observing the microstructure of liver cells showed that lipid droplets were smaller in PFA and PFB than in CON. We confirmed that Fructus Pyri Pyrifoliae extract fermented by lactic-acid bacteria can affect gene expression of leptin, adiponectin, and $TNF-{\alpha}$ in liver cells, showing an obesity treatment effect. From the results above, it was observed that weight gain from increased gene expression in adipose cells as well as from the increased proportion of adipose cells caused by a high-fat diet can be statistically significantly reduced by taking Fructus Pyri Pyrifoliae extract fermented by lactic-acid bacteria. Therefore, Fructus Pyri Pyrifoliae extract fermented by lactic-acid bacteria can be effective for preventing and treating obesity by reducing weight and adipose cells.

• Genomics & Informatics
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• v.8 no.3
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• pp.116-121
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• 2010

The association between adiponectin concentration and obesity have been reported and genetic variations of the ADIPOQ gene are known to influence the plasmatic concentration of adiponectin. Therefore, we investigated the effect of AIPOQ single nucleotide polymorphism (SNP) on obesity-related variables, and their modulation by dietary intakes in Korean women. The subjects consisted of 3,217 Korean women aged 40-59 years participating in the Korean Genome Epidemiology Study (KoGES). The general characteristics, anthropometric variables, serum blood profiles were measured. Dietary intake was analyzed using the Food Frequency Questionnaire. Subjects with the T allele of AIPOQ rs182052 showed significantly higher obesity-related variables such as weight (p=0.005), BMI (p<0.000), fat body mass (p=0.005), and waist-hip ratio (p=0.007) than those with the C allele. Moreover, the rs182052 T allele was associated with an increased risk of obesity prevalence (p=0.019). However, there were not any significant interactions observed between the genotype of ADIPOQ rs182052 and dietary intake on BMI and fat body mass. These findings suggest that the obesity-related variables may be more dominantly affected by the genotype of ADIPOQ rs182052 than dietary intake in middle aged Korean women.

• Journal of Nutrition and Health
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• v.48 no.2
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• pp.133-139
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• 2015

Purpose: There is a fair amount of evidence indicating that increased risk of obesity and insulin resistance is associated with postmenopausal state, but can be modulated by diet and exercise. In this study, we explored whether a Pueraria lobata root-based supplement containing Rehmannia glutinosa (PR) and/or aerobic treadmill exercise can modify the metabolic changes associated with estrogen deficiency. Methods: Seventy rats were randomly assigned to the following groups for 8 weeks (n=10 per group): SHAM, sham-operated; PR0, ovariectomized (OVX) control; PR200, OVX with PR200 mg/kg B.W; PR400, OVX with PR400 mg/kg B.W; EPR0, OVX with exercise; EPR200, OVX with exercise and PR200 mg/kg B.W; EPR400, OVX with exercise and PR400 mg/kg B.W. Results: OVX induced significant increases in body weight, food intake, fat mass, LDL-cholesterol, and fasting blood glucose, confirming induction of menopausal symptoms. PR supplementation or exercise significantly suppressed the above mentioned changes through different regulatory elements in adipose tissue: PR supplement upregulated adiponectin gene expression and aerobic exercise upregulated adiponectin and insulin receptor gene expression and a combination of PR supplement and aerobic exercise showed an additive effect on adiponectin gene expression. Conclusion: Taken together, the results of this study suggest that PR supplement has a potential to provide health benefits in OVX rats through leptin and adiponectin secretion. In addition, the data suggest that combination of exercise and PR would have additive effects on metabolic dysfunction associated with estrogen deficiency.

• Food Science and Preservation
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• v.24 no.4
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• pp.536-541
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• 2017

Hyperglycemia found in diabetes mellitus causes several physiological abnormalities including the formation of advanced glycation end products (AGEs) and oxidative stress. Accumulation of AGEs and elevation of oxidative stress plays major roles in the development of diabetic complications. Adiponectin secreted from adipocytes is known to improve insulin sensitivity and blood glucose level. Curcumin (CCM), a bioactive component of turmeric, has been reported as a potent antioxidant. Present work aimed to elucidate the roles of CCM in high glucose-induced protein glycation and intracellular events in mature adipocytes. The results demonstrated that CCM inhibited the formation of fluorescent AGEs by approximated 52% at 3 weeks of bovine serum albumin (BSA) glycation with glucose. Correspondingly, CCM decreased the levels of fructosamine and ${\alpha}-dicarbonyl$ compounds during BSA glycation with glucose. These data suggested that CCM might be a new promising anti-glycation agent. Also, CCM reduced high glucose-induced oxidative stress in a dose dependent manner, whereas CCM treatment time-dependently elevated the expression of adiponectin gene in 3T3-L1 adipocytes. The findings from this study suggested the possibility of therapeutic use of CCM for the prevention of diabetic complications and obesity-related diseases.