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1.
Arch. endocrinol. metab. (Online) ; 65(2): 126-136, Mar.-Apr. 2021. tab, graf
Article in English | LILACS | ID: biblio-1248811

ABSTRACT

ABSTRACT Objective: There are discrepancies about the relationship of IL-6, clusterin and irisin with obesity and obesity associated insulin resistance and also about their sexual dimorphism. This study aimed at evaluating the circulating levels of IL-6, clusterin and irisin in obese subjects of both sexes who had different grades of obesity and examining their sexual dimorphism and their association with insulin resistance. Subjects and methods: This study included 176 non-diabetic subjects of both sexes who were classified according to their sex into two groups; the male and the female groups. The male group (88 men) was classified according to BMI into; group 1 (22 lean men), group 2 (22 class I obese men), group 3 (22 class II obese men) and group 4 (22 class III obese men). The female group (88 women) was classified according to BMI exactly as the male group. Metabolic parameters, IL-6, clusterin, and irisin levels were measured. Data were analyzed by ANOVA test, post hoc Tukey's test and independent t-test. Pearson correlation was used to assess the association between variables. Results: In obese subjects of both sexes, circulating IL-6, clusterin and irisin levels were significantly elevated and positively correlated with HOMA-IR. Obese males showed significantly higher HOMA-IR, IL-6, clusterin and irisin levels than obese females. Conclusion: Obesity in both sexes, especially in males was associated with high levels of IL-6, clusterin and irisin and worsened the metabolic pattern. Circulating IL-6, clusterin and irisin may represent possible therapeutic targets for insulin resistance in obese subjects.


Subject(s)
Humans , Male , Female , Insulin Resistance , Fibronectins/blood , Interleukin-6/blood , Sex Characteristics , Clusterin/blood , Obesity/blood , Body Mass Index , Obesity/classification
2.
Article in English | IMSEAR | ID: sea-163494

ABSTRACT

Aim: This study aimed to evaluate the effect of magnesium supplement to atorvastatin on hyperlipidemic patients and to elucidate the possible ability of oral magnesium supplement to counteract or delay statins induced myalgia. Study Design: Forty hyperlipidemic male and female patients were randomly divided into two groups: group one consisted of twenty patients, who received atorvastatin 10 mg once daily for 6 weeks then 20 mg once daily for another 6 weeks; group two consisted of twenty patients, who received the same dose of atorvastatin plus once daily oral low dose magnesium sulfate trihydrate 419.5 mg equivalent to 50 mg of magnesium. Place and Duration of Study: The Laboratory of Pharmaceutical Research Center of Faculty of Pharmacy, Tanta University, Egypt, between July to December 2013. Methodology: Two samples of venous blood (2 ml + 8 ml =10 ml total), were collected from all individuals, and were drawn from the antecubital vein before, 1.5 and 3 months after treatment. Sera and plasma were separated immediately for biochemical analyses of lecithin cholesterol acyltransferase (L-CAT) (ELISA), creatine kinase (CK), serum Ca+, Mg++, Na+, K+, lipid profile and aspartate transaminase (AST) (colorimetrically), and serum creatinine (S.Cr) spectrophotometrically. Results: The statistical analysis revealed that, 3 months after treatment, both groups showed significant amelioration in lipid profiles and significant elevation in L-CAT level regarding to baseline data obtained before initiation of treatment. In addition, the patients received atorvastatin plus magnesium supplement showed significantly higher levels of serum magnesium, plasma L-CAT and HDL-cholesterol concentrations and significantly lower total cholesterol, LDL-cholesterol and triglycerides concentrations with non significant lower CK level as compared to the patients group received atorvastatin solely. Conclusion: Mg++ supplement to atorvastatin improve all lipid profile and provide better control on dyslipidemia than atorvastatin alone. However, Mg++ supplement to atorvastatin doesn’t prevent elevation in CK; it may delay and provide some protection against statin induced myopathy that in turn may increase patient compliance.

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