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  1. Chin KY, Ima-Nirwana S, Mohamed IN, Aminuddin A, Ngah WZ
    Exp. Clin. Endocrinol. Diabetes, 2013 Jul;121(7):407-12.
    PMID: 23765753 DOI: 10.1055/s-0033-1345164
    Testosterone and sex hormone-binding globulin (SHBG) have been shown to be associated with metabolic syndrome (MS) in men. This study aimed at validating these relationships in a group of middle-aged and elderly men and assessing their strength of association to MS. A cross-sectional study of 332 Malaysian men aged 40 years and above was conducted. The blood of subject was collected under fasting condition for determination of testosterone, SHBG, glucose and lipid levels. Their medical history, smoking and alcohol consumption status, waist circumference (WC), body mass index (BMI) and blood pressure (BP) were recorded. All testosterone and SHBG levels were significantly reduced in MS subjects compared to non-MS subjects (p<0.05). Testosterone and SHBG were correlated significantly with most of the MS indicators without adjustments. In multiple regression analysis, the triglyceride level was the only MS indicator that was significantly, inversely and independently associated with all testosterone measurements and SHBG (p<0.05). Waist circumference was significantly and negatively associated with SHBG level (p<0.05) though not independent of BMI. Total testosterone and SHBG were significantly and inversely associated with the presence of MS. Testosterone and SHBG are potential intervention targets for the prevention of MS in men.
    Matched MeSH terms: Metabolic Syndrome X/pathology
  2. Arshad N', Lin TS, Yahaya MF
    CNS Neurol Disord Drug Targets, 2018;17(8):595-603.
    PMID: 30047340 DOI: 10.2174/1871527317666180724143258
    BACKGROUND & OBJECTIVE: Metabolic syndrome (MetS) is an interconnected group of physiological, biochemical, clinical and metabolic factors that directly increase the risk of cardiovascular disease, type 2 diabetes mellitus (T2DM) and mortality. Rising evidence suggests that MetS plays a significant role in the progression of Alzheimer's disease and other neurodegenerative diseases. Nonetheless, the factors linking this association has not yet been elucidated. As we are facing an increasing incidence of obesity and T2DM in all stages of life, understanding the association of MetS and neurodegenerative diseases is crucial to lessen the burden of the disease.

    CONCLUSION: In this review, we will discuss the possible mechanisms which may relate the association between MetS and cognitive decline which include vascular damages, elevation of reactive oxygen species (ROS), insulin resistance and low-grade inflammation.

    Matched MeSH terms: Metabolic Syndrome X/pathology*
  3. Tan EX, Lee JW, Jumat NH, Chan WK, Treeprasertsuk S, Goh GB, et al.
    Metabolism, 2022 01;126:154911.
    PMID: 34648769 DOI: 10.1016/j.metabol.2021.154911
    BACKGROUND: A significant proportion of the non-alcoholic fatty liver disease (NAFLD) population is non-obese. Prior studies reporting the severity of NAFLD amongst non-obese patients were heterogenous. Our study, using data from the largest biopsy-proven NAFLD international registry within Asia, aims to characterize the demographic, metabolic and histological differences between non-obese and obese NAFLD patients.

    METHODS: 1812 biopsy-proven NAFLD patients across nine countries in Asia assessed between 2006 and 2019 were pooled into a curated clinical registry. Demographic, metabolic and histological differences between non-obese and obese NAFLD patients were evaluated. The performance of Fibrosis-4 index for liver fibrosis (FIB-4) and NAFLD fibrosis score (NFS) to identify advanced liver disease across the varying obesity subgroups was compared. A random forest analysis was performed to identify novel predictors of fibrosis and steatohepatitis in non-obese patients.

    FINDINGS: One-fifth (21.6%) of NAFLD patients were non-obese. Non-obese NAFLD patients had lower proportions of NASH (50.5% vs 56.5%, p = 0.033) and advanced fibrosis (14.0% vs 18.7%, p = 0.033). Metabolic syndrome in non-obese individuals was associated with NASH (OR 1.59, 95% CI 1.01-2.54, p = 0.047) and advanced fibrosis (OR 1.88, 95% CI 0.99-3.54, p = 0.051). FIB-4 performed better than the NFS score (AUROC 81.5% vs 73.7%, p 

    Matched MeSH terms: Metabolic Syndrome X/pathology*
  4. Mamikutty N, Thent ZC, Sapri SR, Sahruddin NN, Mohd Yusof MR, Haji Suhaimi F
    Biomed Res Int, 2014;2014:263897.
    PMID: 25045660 DOI: 10.1155/2014/263897
    Metabolic syndrome can be caused by modification of diet by means of consumption of high carbohydrate and high fat diet such as fructose.
    Matched MeSH terms: Metabolic Syndrome X/pathology*
  5. Gan YL, Fu JY, Lai OM, Chew BH, Yuen KH, Teng KT, et al.
    Sci Rep, 2017 09 14;7(1):11542.
    PMID: 28912593 DOI: 10.1038/s41598-017-11813-w
    Tocotrienols, the unsaturated form of vitamin E, were reported to modulate platelet aggregation and thrombotic mechanisms in pre-clinical studies. Using a Food and Drug Administration (FDA)-approved cartridge-based measurement system, a randomised, double-blind, crossover and placebo-controlled trial involving 32 metabolic syndrome adults was conducted to investigate the effect of palm-based tocotrienols and tocopherol (PTT) mixture supplementation on platelet aggregation reactivity. The participants were supplemented with 200 mg (69% tocotrienols and 31% α-tocopherol) twice daily of PTT mixture or placebo capsules for 14 days in a random order. After 14 days, each intervention was accompanied by a postprandial study, in which participants consumed 200 mg PTT mixture or placebo capsule after a meal. Blood samples were collected on day 0, day 14 and during postprandial for the measurement of platelet aggregation reactivity. Subjects went through a 15-day washout period before commencement of subsequent intervention. Fasting platelet aggregation reactivity stimulated with adenosine diphosphate (ADP) did not show substantial changes after supplementation with PTT mixture compared to placebo (p = 0.393). Concomitantly, changes in postprandial platelet aggregation reactivity remained similar between PTT mixture and placebo interventions (p = 0.408). The results of this study highlight the lack of inhibitory effect on platelet aggregation after short-term supplementation of PTT mixture in participants with metabolic syndrome.
    Matched MeSH terms: Metabolic Syndrome X/pathology*
  6. Wong SK, Chin KY, Suhaimi FH, Ahmad F, Jamil NA, Ima-Nirwana S
    Biomed Pharmacother, 2018 Feb;98:191-200.
    PMID: 29257979 DOI: 10.1016/j.biopha.2017.12.042
    This study aimed to investigate the bone quality in rats induced with metabolic syndrome (MetS) using high-carbohydrate high-fat (HCHF) diet. Male Wistar rats (n = 14) were randomized into two groups. The normal group was given standard rat chow. The MetS group was given HCHF diet. Diet regimen was assigned for a period of 20 weeks. Metabolic syndrome parameters were measured monthly until MetS was established. Left tibiae were scanned using micro-computed tomography at week 0, 8, 12, 16, and 20 to analyze the trabecular and cortical bone structure. At the end of the study, rats were euthanized and their bones were harvested for analysis. Metabolic syndrome was established at week 12 in the HCHF rats. Significant deterioration of trabecular bone was observed at week 20 in the HCHF group (p  0.05). Femur length and width in the HCHF group were significantly shorter than the normal group (p 
    Matched MeSH terms: Metabolic Syndrome X/pathology
  7. Pung YF, Chilian WM, Bennett MR, Figg N, Kamarulzaman MH
    Am J Physiol Heart Circ Physiol, 2017 Mar 01;312(3):H541-H545.
    PMID: 27986661 DOI: 10.1152/ajpheart.00653.2016
    Although there are multiple rodent models of the metabolic syndrome, very few develop vascular complications. In contrast, the JCR:LA-cp rat develops both metabolic syndrome and early atherosclerosis in predisposed areas. However, the pathology of the normal vessel wall has not been described. We examined JCR:LA control (+/+) or cp/cp rats fed normal chow diet for 6 or 18 mo. JCR:LA-cp rats developed multiple features of advanced cystic medial necrosis including "cysts," increased collagen formation and proteoglycan deposition around cysts, apoptosis of vascular smooth muscle cells, and spotty medial calcification. These appearances began within 6 mo and were extensive by 18 mo. JCR:LA-cp rats had reduced medial cellularity, increased medial thickness, and vessel hypoxia that was most marked in the adventitia. In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia.NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN.
    Matched MeSH terms: Metabolic Syndrome X/pathology
  8. Wickramatilake CM, Mohideen MR, Pathirana C
    Ann Endocrinol (Paris), 2015 Jul;76(3):260-3.
    PMID: 26142486 DOI: 10.1016/j.ando.2015.04.008
    OBJECTIVE: There is limited data on the assessment of relationship between sex hormones, metabolic syndrome (MS) and inflammation. Therefore, our objective was to examine the relationship between metabolic syndrome, testosterone and inflammation.
    PATIENTS AND METHODS: It was a cross-sectional study which included 309 subjects in the age range of 30-70years. Blood was analyzed for plasma glucose, serum lipids, total testosterone (TT) and high-sensitivity C-reactive protein (hs-CRP).
    RESULTS: There were 153 patients with metabolic syndrome and 156 without MS according to modified NCEP guidelines. Age, BMI, obesity, dyslipidaemia, smoking (OR=2.35, CI=1.35-4.09), LDL-Ch, low TT (OR=0.76, CI=0.38-1.52) and elevated hs-CRP (OR=1.56, CI=0.87-2.80) were significant independent predictors of MS (all P<0.05).
    CONCLUSIONS: The low testosterone and high hs-CRP levels are independent predictors of metabolic syndrome.
    KEYWORDS: Hommes; Inflammation; Men; Metabolic syndrome; Syndrome métabolique; Testosterone; Testostérone
    Matched MeSH terms: Metabolic Syndrome X/pathology
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