scholarly journals Adipose Tissues Characteristics of Normal, Obesity, and Type 2 Diabetes in Uygurs Population

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Jun Zhang ◽  
Zhiwei Zhang ◽  
Yulei Ding ◽  
Peng Xu ◽  
Tingting Wang ◽  
...  

Our results showed that, at the same BMI level, Uygurs have greater WHR values, abdominal visceral fat content, and diabetes risks than Kazaks. In addition, values of HDL-C in Uygur subjects were lower than those in Kazak subjects, and values of creatinine, uric acid, diastolic blood pressure, blood glucose, and fructosamine in Uygur male subjects were lower than those in Kazak male subjects. In contrast, systolic blood pressure values in Uygur subjects were greater than those in Kazak subjects, and blood glucose values were greater in Uygur female subjects than in Kazak female subjects. Additionally, in Uygurs, visceral adipose tissue expression levels ofTBX1andTCF21were greater in obesity group than in normal and T2DM groups and lower in T2DM group than in normal group (P<0.01). The visceral adipose tissue expression levels ofAPNin normal group was greater than those in obesity and T2DM groups, and visceral adipose tissue expression levels ofTNF-αandMCP-1in normal group were lower than those in obesity and T2DM groups (P<0.01). In conclusion, T2DM in Uygurs was mainly associated with not only distribution of adipose tissue in body, but also change in metabolic activity and adipocytokines secretion of adipose tissue.

2012 ◽  
Vol 1 (2) ◽  
pp. 68-73
Author(s):  
R Eldeeb ◽  
MH Gamal-Eldin ◽  
EA Khowailed ◽  
MM Fathy ◽  
N Shantakumari ◽  
...  

Background: The excess usage of fructose as a sweetener has raised the incidence of insulin resistance among the population which is associated with dyslipedemia, hypertension and obesity. This work studied the effect of induced insulin resistance on body weight, blood pressure, lipid profile, glycemic state and lipolytic activity of adipose tissue in male rats. Methods: Twenty male rats of 129.4 g average body weight (BW) were divided equally into two groups. Both had free access to water. The control group had pure water; the experimental group had water mixed with 25% of fructose to induce insulin resistance. After 3 months body weight, blood pressure, fasting blood glucose, insulin levels, lipid profile of both groups were measured and lipolytic activity of adipose tissue was assessed. Results: Rats given fructose for 3 months showed significant increase in BW, systolic blood pressure, triglyceride, Cholesterol, low density lipoprotein, fasting blood glucose and insulin levels with a significant decline in highdensity lipoprotein. Lipolytic activity of subcutaneous (SC) and visceral adipose tissue in presence of adrenaline increased significantly which runs in parallel with the results obtained in presence of insulin as it showed a significant rise in both SC and visceral adipose tissue. Data were considered statistically significant at alpha level of 5%. Conclusion: Insulin resistance induced in male rat by high fructose consumption showed a significant rise in BW and is associated with hypertension and dyslipidemia with significant rise in lipolytic activity of both SC and visceral adipose tissue. DOI: http://dx.doi.org/10.3126/njms.v1i2.6602 Nepal Journal of Medical Sciences. 2012;1(2): 68-73


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sathish Babu B Vasamsetti ◽  
xinyi zhang ◽  
Emillie M Coppin ◽  
Jonathan Florentin ◽  
Sasha Koul ◽  
...  

Introduction: Myocardial infarction (MI) is the major cause of morbidity and mortality in the western world. Insulin resistance is a major complication in patients with MI. Hypothesis: Loss of visceral adipose tissue (VAT) resident macrophages in MI results in diminished adiponectin production causing systemic insulin resistance. Methods: To understand if MI results in insulin resistance, we analyzed UPMC patient records and identified patients who had normal fasting blood glucose levels on average 15 days before ST elevation myocardial infarction (STEMI) and checked their fasting blood glucose levels 30 days after STEMI. To understand the mechanisms of MI-induced insulin resistance, we used a mouse model of coronary ligation in C57BL/6 mice and analyzed the features of insulin resistance by measuring serum insulin, serum adiponectin, AKT activation status in the liver and muscle. Results: We found that 50% of non-diabetic patients (fasting blood glucose levels 99±2.5 mg/ dl) developed hyperglycemia (141±13 mg/dl) after MI, suggesting that MI causes insulin resistance. Consistently, mice with MI had higher fasting blood insulin, and reduced p-Akt levels in the liver and skeletal muscles confirming insulin resistance. Concomitantly, mice and patients with MI had reduced number of visceral adipose tissue (VAT) resident macrophages. In line with this, MI resulted in marked reduction in the level of macrophage colony stimulating factor (M-CSF), a cytokine required for tissue resident macrophage survival. M-CSF supplementation in mice with MI improved insulin sensitivity and decreased inflammatory phenotype of VAT macrophages. Furthermore, the systemic level of adiponectin, which is reported to augment insulin sensitivity, was profoundly reduced in mice after MI. Specific depletion of VAT resident macrophages resulted in lower levels of adiponectin in the serum, indicating that this macrophage subset is necessary for adiponectin production by adipocytes. Conclusions: Our data demonstrate that diminished M-CSF levels after MI triggers apoptosis of VAT resident macrophages, resulting in reduced adiponectin secretion and systemic insulin resistance.


2008 ◽  
Vol 18 (6) ◽  
pp. 695-701 ◽  
Author(s):  
Victoria Catalán ◽  
Javier Gómez-Ambrosi ◽  
Carlos Pastor ◽  
Fernando Rotellar ◽  
Camilo Silva ◽  
...  

2009 ◽  
Vol 19 (6) ◽  
pp. 771-776 ◽  
Author(s):  
Victoria Catalán ◽  
Javier Gómez-Ambrosi ◽  
Amaia Lizanzu ◽  
Amaia Rodríguez ◽  
Camilo Silva ◽  
...  

2017 ◽  
Vol 42 (12) ◽  
pp. 1254-1263 ◽  
Author(s):  
Maja Bundalo ◽  
Ana Djordjevic ◽  
Biljana Bursac ◽  
Maja Zivkovic ◽  
Goran Koricanac ◽  
...  

The adipose tissue renin–angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by a fructose-rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocyte nuclear membranes possess angiotensin receptor types 1 and 2 (AT1R and AT2R), which couple to nuclear signaling pathways and regulate oxidative gene expression under FRD conditions. We analyzed the effect of consumption of 10% fructose solution for 9 weeks on biochemical parameters, adipocyte morphology, and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NADPH oxidase 4 (NOX4), matrix metalloproteinase-9 (MMP-9), and manganese superoxide dismutase (MnSOD) in adipose tissue of Wistar rats. We detected AT1R and AT2R in the nuclear fraction. FRD reduced the level of angiotensin receptors in the nucleus, while increased AT1R and decreased AT2R levels were observed in the plasma membrane. FRD increased the ATRAP mRNA level and decreased MnSOD mRNA and protein levels. No significant differences were observed for MMP-9 and NOX4 mRNA levels. These findings coincided with hyperleptinemia, elevated blood pressure and triglycerides, and unchanged visceral adipose tissue mass and morphology in FRD rats. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study demonstrates the different effects of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidant capacity in visceral fat of fructose-fed rats were accompanied by an increased AT1R level in the plasma membrane, while upregulation of ATRAP and a decrease of nuclear membrane AT1R suggest an increased capacity for attenuation of excessive AT1R signaling and visceral adiposity.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Amanda A Soler ◽  
Brenda Hutcheson ◽  
Jenny Yang ◽  
Chastity Bradford ◽  
Frank F Zhang ◽  
...  

Increased intra-abdominal (visceral) adipose tissue is a key feature of the metabolic syndrome affecting over 30% of the U.S. population. Expansion of visceral adipose tissue is linked to the development of hypertension and is a risk factor for cardiovascular disease that can ultimately lead to end-organ damage. While reduction in visceral adipose tissue volume offers cardioprotective effects, the cardiovascular mechanisms behind these beneficial effects remain unclear. In this study, we removed ~90% of visceral adipose tissue (=~5% body weight) by intra-abdominal lipectomy and assessed large arterial stiffness, large artery structural matrix components, and blood pressure in a metabolic syndrome rat model (JCR:LA-cp, JCR). Large artery stiffness was significantly elevated in JCR vs. normal (Sprague Dawley, SD) rats (75±2% JCR vs. SD (carotid)) with a concomitant significant increase in MMP12-dependent elastin degradation (3-6 fold vs. SD). Intra-abdominal lipectomy normalized large artery stiffness, blocked MMP12 activation and reduced elastin degradation in JCR animals (~75% (carotid) vs. untreated JCR). Likewise, hypertension in JCR animals was significantly attenuated by intra-abdominal lipectomy (MABP=156±3 mmHg JCR vs. 90±6 mmHg SD vs. 132±4 mmHg JCR+lipectomy). 20-hydroxyeicosatetraeonic acid (20-HETE), an arachidonic acid metabolite known to be a potent vasoconstrictor in resistance arteries, was significantly elevated in the visceral adipose tissue of JCR rats (~6 fold vs. SD). Intra-abdominal lipectomy normalized 20-HETE levels in JCR rats. Like intra-abdominal lipectomy, 20-HETE antagonists restored large artery elasticity, blocked MMP12 activation and elastin degradation, and significantly decreased blood pressure (125±3 mmHg JCR+20-HETE antagonists) in JCR rats. Thus, 20-HETE may be an important adipokine that mediates the adverse effects of expanded visceral fat volume in the metabolic syndrome and its inhibition may provide a pharmacological approach for the management of central obesity-driven large artery stiffness and hypertension.


2003 ◽  
Vol 62 (3) ◽  
pp. 149-157 ◽  
Author(s):  
Nobuyuki Miyatake ◽  
Kayo Takahashi ◽  
Jun Wada ◽  
Hidetaka Nishikawa ◽  
Akie Morishita ◽  
...  

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