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Hyperandrogenism and hyperinsulinemia have resulted from dysfunction of the theca cell of the ovary and adipose tissue and each one potentiates the other in patients with androgen excess disorders e.g., polycystic ovary disease and idiopathic hirsutism. Possible external and/or internal triggers can produce such cellular dysfunction. There is evidence that sodium valproate acts as a trigger of cellular dysfunction and produces both hyperinsulinemia and hyperandrogenism. Therefore, the elimination of these triggers can help the patients to recover from hyperinsulinemia, insulin resistance and hyperandrogenism.  相似文献   
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Background and study aimsPatients with non-alcoholic fatty liver disease (NAFLD) exhibit features of metabolic syndrome, including a high body mass index, central obesity, high blood pressure, and abnormal lipid profile values. Orlistat, an intestinal lipase enzyme inhibitor, improves insulin resistance. We aimed to investigate the effects of short-term therapy with orlistat on the components of metabolic syndrome associated with NAFLD and explore its effect on liver fibrosis scores.Patients and methodsAn open-label placebo-controlled clinical study using orlistat for 12 weeks was carried out on 50 patients with NAFLD. They were divided into a placebo group (Group I) and an orlistat treatment group (120 mg per day, Group II). The diagnosis of NAFLD was made by ultrasonography and laboratory investigations. Anthropometric and blood pressure measurements and hepatic liver enzymes, fasting lipids, and blood glucose levels were determined before and after treatment. Lipid indices including cholesterol (Chol-I), triglyceride (TG-I), triglyceride-glucose (TYG-I), and the scores for lipid fibrosis using the NAFLD fibrosis score (NFS) and Fibrosis-4 score (Fib-4) were also determined.ResultsOrlistat significantly improved the anthropometric and metabolic indices (TG-I, TYG-I) and liver enzymes. Orlistat demonstrated a favorable impact on the NAS and Fib-4 scores for liver fibrosis.ConclusionOrlistat improves the components of metabolic syndrome, leading to the improvement of insulin resistance and thereby improves fatty infiltration of the liver. To a lesser extent, orlistat improved the liver fibrosis scores.  相似文献   
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AIMS:

Patients with type-2 diabetes mellitus have greater carotid intima media thickness and they are at risk for generalized atherosclerosis. This study aimed to compare the thickness of carotid artery intima media in type-2 diabetes mellitus patients with and without nonblood pressure component metabolic syndrome.

SETTINGS AND DESIGN:

This was a comparative observational study conducted in the Departments of Pharmacology and Physiology in the College of Medicine, Al-Mustansiriyia University in cooperation with Baghdad Teaching Hospital.

MATERIALS AND METHODS:

Forty-six diabetic patients of both sexes with systolic blood pressure < 130 mm Hg and diastolic blood pressure < 85 mm Hg were subjected to high resolution B-mode ultrasonography of the common and internal carotid arteries. Patients were grouped into those without metabolic syndrome (Group I) and with nonblood pressure component metabolic syndrome (Group II).

STATISTICAL ANALYSIS:

The two-tailed unpaired Student''s t-test was used in this study.

RESULTS:

Significantly high mean thickness was observed in the common carotid intima media (0.824 ± 0.155 mm) but not in the internal carotid arteries in group II patients compared to group I patients (0.708 ± 0.113 mm). Group II also had a significant number of patients with increased lesion intima media thickness (≥ 1.1 mm).

Conclusion:

The greater carotid intima media thickness observed in type 2 diabetes mellitus patients is related to the metabolic syndrome even in the absence of the blood pressure component.  相似文献   
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Anti-cyclic citrullinated peptide (ACCP) autoantibodies are likely to be involved in the development of rheumatoid arthritis in at least 70 % of the patients. These autoantibodies are associated with type 1 diabetes and may predict the development of rheumatoid arthritis in later life. This study aimed to examine the association between interleukin-6 (IL-6), a proinflammatory cytokine, highly sensitive C-reactive protein (hsCRP), and ACCP autoantibodies in type 2 diabetes (T2D) patients without past or current history of arthropathy taking in consideration the age-effect factor. A total number of 70 T2D patients and 60 healthy subjects were recruited from the center of diabetes in Erbil, Iraq. The patients were grouped into two: group I (age 35–45 years): group IA, healthy subjects and group IB, diabetic patients; group II (age ≥60 years): group IIA, healthy subjects and group IIB, diabetic patients. Fasting serum glucose, HbA1c%, lipid profile, IL-6, hsCRP, and ACCP autoantibodies were determined. Significant alterations in lipid profile were observed in group IIB compared with group IB. Patients of group IIB have significant high serum IL-6 (458.3 ± 43.04 pg/ml), hsCRP (5.576 ± 0.643 mg/L), and ACCP autoantibodies (74.31 ± 8 U/ml) than corresponding group IB: IL-6 (381.4 ± 22.6 pg/ml), hsCRP (4.92 ± 0.343 mg/L), and ACCP (49.43 ± 7.09 U/ml). Significant positive correlation (r = 0.445) between serum IL-6 and ACCP autoantibodies was observed only in group IB. It concludes that proinflammatory markers and autoantibodies that related to arthritis are increased in old diabetic patients compared with younger age, and IL-6 correlated with ACCP autoantibodies in younger patients which indicated age effect.

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Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the growth of several cancer cell lines. The aim of this study is to compare the cytotoxic effect of aspirin with diclofenac on the growth of HeLa cell, mammary cell carcinoma, rhabdomyosarcoma and fibroblast cell lines in the culture media. The cells are cultured in RPMI-1640 culture media supplemented with 5% fetal calf serum and antibiotics. Aspirin (5 mg/well) and diclofenac (0.625 mg/well) significantly inhibit the growth of HeLa, rhabdomyosarcoma and fibroblast cells. The cytotoxic effect of aspirin against rhabdomyosarcoma is significantly (p < 0.001) higher than that of diclofenac with a potency approximated 2.6. It concludes that aspirin and diclofenac inhibit the growth of fibroblast and cancer cell by inhibiting the up-regulation of cyclooxygenases enzymes in cancer cells. Aspirin is more effective than diclofenac against the growth of rhabdomyosarcoma cell line.  相似文献   
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