Journal of Metabolic Syndrome

Objective: While diet and exercise reduce the risk of cardiovascular morbidity in overweight populations, the effects of combined aerobic and resistance training on arterial health has not been comprehensively examined.

Methods: We investigated changes in both central and peripheral arterial stiffness using carotid artery distensibility and carotid to radial pulse wave velocity (PWVc-r), respectively, in twenty-five overweight, young women who participated in 16-weeks of 5-7 d/wk aerobic exercise, 2 d/wk resistance training, and hypo-caloric diet intervention. Pro-Collagen Type I C-Peptide (PIP) was used as a marker of type I collagen synthesis and C-telopeptide of type I collagen (CTX), a marker of type I collagen degradation.

Results: Carotid artery distensibility was unaltered (Pre: 5.1×10-3 ± 3.9×10-4 vs. Post: 5.5×10-3 ± 3.5×10-4, p=0.26); however, PWVc-r increased following the intervention (Pre: 8.1 ± 0.3 m/s vs. Post: 8.9 ± 0.3 m/s, p<0.05). There were no changes in PIP (Pre: 1188 ± 91 ng/mL vs. Post: 1222 ± 94 ng/mL, p = 0.69), however, CTX increased with the intervention (0.65 ± 0.01 ng/mL vs. Post: 0.80 ± 0.02 ng/mL, p<0.001). There were no relationships between markers of collagen turnover and arterial stiffness measures.

Conclusion: The intervention did not alter carotid artery distensibility or circulating markers of type I collagen synthesis but was associated with increased PWVc-r and CTX. Therefore, 16-weeks of diet and combined aerobic and resistance training may lead to increased peripheral artery stiffness, as measured by PWVc-r, however, cardiovascular risk assessed by carotid artery distensibility remained unchanged.

Background & objectives: Effects of statins on serum lipids in hyperlipidemia are not well defined. We compared the effects of atorvastatin and niacin, alone and combination, on lowering serum LDL-C and Lp (a) and increasing HDL-C in hyperlipidemia patients.

Patients and methods: A total of 150 adult patients (Group-A) with hyperlipidemia and 100 normal adults controls (Group-B) were included in the study. The fasting blood samples were taken and serum (I°) were stored frozen until analysed for TG, TC, LDL-C, HDL-C, and Lp (a). The 50 patients (Group A1) were prescribed Atorvastatin (10 mg once daily for 3 months), 50 patients (Group A2) were prescribed Niacin (50 mg twice daily for 3 months) and 50 patients (Group A3) were prescribed combination of the two drugs with same doses for 3 months. Blood samples were taken again at follow up and serum (II°) was stored frozen until analysed for lipids by biochemical methods.

Results: Lipid parameters (mg/dl), i.e. TG, TC, LDL-C, & Lp(a), were raised and HDL-C was reduced in patients (Group-A) compared to controls (Group-B); Atovastatin (10 mg/ day) and Niacin (50 mg/2day) significantly lowered TG,TC, LDL-C & Lp(a) and raised HDL-C in Group A1 and Group A2 respectively; Combination therapy (atorvastatin: 10 mg/day + Niacin : 50 mg*2/day) was much more effective in lowering TG, TC, LDL-C & LP(a) and raising HDL-C in Group A3.

Conclusions: The effects of combination therapy of the two drugs were much higher than their effects alone and therefore, can be adopted in hyperlipidemia patients.

Background: Metabolic Syndrome (MetS) is associated with elevated risk of diabetes, cardiovascular disease, and premature mortality. To date, however, the association between MetS and obesity-related cancers has not been systematically assessed within a population-based sample.

Methods: In order to quantify the association between MetS and its components on any-site, breast, prostate, and colon cancers, data from the U.S. NHANES 1999-2010 (n=15 141, 18-85 years) were used.

Results: In general, the prevalence of MetS was higher amongst those with a self-reported history of cancer. Although MetS, its individual components, and total number of components were positively related to odds of any-site, breast, prostate, and colon cancers, this effect was almost entirely eliminated after adjustment for age. In age-adjusted models, elevated blood glucose was associated with higher odds of prostate (OR: 1.67, 95% CI: 1.08-2.56) and colon cancer (OR: 1.60, 95% CI: 1.02-2.53), and a protective effect of low HDL cholesterol on prostate cancer (OR: 0.64, 95% CI: 0.43-0.94). Further adjustment for sex, ethnicity, income, education, smoking, alcohol, and recreational/ leisure-time physical activity had only minimal influence on these associations. In multivariable analyses, no uniform linear trends were observed between the number of MetS components and site-specific cancers.

Conclusion: After accounting for covariates, no consistent association between MetS and any-site, breast, prostate, or colon cancer was observed. Further prospective study is necessary to confirm and extend our understanding of the role of age and other risk factors on the inter-relationship between metabolic health and cancer.

Aim: The aim of the current study was to investigate the associations between rs3732581, rs73887537 of PARL gene with type 2 diabetes mellitus and its related phenotypes in Chinese T2DM case-control population.

Methods: We genotyped PARL gene rs3732581, rs73887537 polymorphisms in 543 T2DM patients and 384 healthy controls by using PCR-RFLP technique. Plasma glucose, insulin and lipid were measured by biochemical technique.

Results: rs73887537 polymorphism of PARL gene was not existed in the studied population. The genotype and allele distributions of rs3732581 polymorphism were not significantly different between T2DM and control groups (both P>0.05). However compared with carriers of C allele, the carriers of the GG genotype showed significantly higher levels of triglyceride, total cholesterol in the T2DM and control groups respectively.

Conclusion: rs73887537 polymorphism of PARL gene was not existed in the Chinese studied population. The rs3732581 polymorphism of PARL gene is not associated with the presence of T2DM. However, it is associated with blood lipid levels in T2DM and healthy Chinese population differently.

Background: Metabolic Syndrome (MetS) is a cluster of factors that increase the risk of Coronary Artery Disease (CAD) and Diabetes Mellitus (DM).

Methods: A cross-sectional analysis of data was performed from 355 patients who attended rural Malaysian district hospital outpatient clinics from January to June 2011, using the International Diabetes Federation (IDF) criteria to define MetS and identify the demographic risk factors for developing MetS.

Results: Prevalence MetS was 48.7% of which 63.6% were female. Hypertension was the most common metabolic risk factor (82.4%). Age, female sex and BMI were significant factors for developing MetS with OR=1.05 (CI=1.03- 1.06), 2.53 (CI=1.51-4.26) and 1.19 (CI=1.13-1.25) respectively. Risk was significantly lower among Chinese patients compared to Indian patients p=0.01, OR=0.46 (CI=0.23-0.87).

Conclusion: Age, female gender and ethnicity were noted to be demographic factors for developing MetS.

Metabolic syndrome is defined as a constellation of metabolic disturbances that coexist in a subject. Due to its complex multi factorial etiology, metabolic syndrome causes damage to different organs, representing an increasing and significant global burden. Insulin resistance plays a central role in metabolic syndrome pathogenesis and underpins the majority of metabolic impairments, including the organ diseases that originate from metabolic syndrome. Regarding white adipose tissue, an altered adipokines profile in obesity characterizes a proinflammatory state, which is implicated in the pathogenesis of liver and cardiac disorders. Regarding the liver, nonalcoholic fatty liver disease is a benign disease that can progress towards liver fibrosis in the presence of persistent inflammation and increased oxidative stress. Concerning cardiovascular diseases, adipokines, reactive oxygen species and over activity of the renin angiotensin system play central roles. Another target organ of metabolic syndrome is the ovary, where polycystic ovary syndrome is also related to insulin resistance and can originate from adverse intrauterine conditions. The notion that maternal obesity can trigger metabolic syndrome in the fetus is alarming, given that it can be passed to other generations even if adequate nutrition is provided after birth. This review aimed to assess the main outcomes of metabolic syndrome in white adipose tissue focusing on insulin resistance and adipokines, the cardiovascular system, the liver and ovaries as well as fetal origins; this review also discusses some proposed pharmacological treatments to provide a better understanding of the related pathways in these secondary findings

Background: MicroRNAs (miRNAs) have emerged as an important class of small molecules that regulate a spectrum of biological processes. However, their roles in the regulation of lipid metabolism and inflammatory response in metabolic syndrome are not completely known. To identify miRNAs and investigate how they are involved in lipid metabolism and inflammatory response in cells and animals and define the function and regulatory mechanism of these microRNAs.

Methods and results: We stimulated human THP-1 macrophages with oxLDL and found that one of the miRNAs, miR-150, strongly responded to the lipid accumulation and inflammatory response in these cells. Overexpression of miR-150 in macrophage cells resulted in an increase in lipid accumulation, accompanying with a high expression of several pro-inflammatory cytokines. Conversely, when miR-150 knockout mice were challenged with a high fat diet, these mice presented reduced whole body weight with less fat accumulation, improved systemic glucose tolerance and insulin sensitivity. The expression of pro-inflammatory cytokines in the insulin target adipose tissues was reduced in miR-150 null mice. We identified Adiponectin receptor 2 (AdipoR2) as a potential miR-150 target gene and suggested it may play an important role in miR-150-mediated lipid metabolism and inflammatory response.

Conclusions: These results uncovered novel functions for miR-150 in modulating lipid metabolism and inflammatory response by regulating genes linked to lipid accumulation and related inflammation and provided a firm mechanistic explanation with characterization and determination of critical miR-150 for its associations with the metabolic diseases. These studies will highly impact and benefit metabolic disease research both in vitro and in vivo