Gregory P Bondy

University of British Columbia - Vancouver, Vancouver, British Columbia, Canada

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Publications (7)25.31 Total impact

  • Article: Ethnic variation in fat and lean body mass and the association with insulin resistance.
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    ABSTRACT: Body fat distribution varies among different ethnic groups, yet less is known regarding differences in lean mass and how this may affect insulin resistance. Our objective was to compare total body fat to lean mass ratio (F:LM) in Aboriginal, Chinese, European, and South Asian individuals with differences in insulin resistance. PARTICIPANTS, DESIGN, AND SETTING: Aboriginal (196), Chinese (222), European (202), and South Asian (208) individuals were recruited across a range of body mass index to participate in this cross-sectional community study. Total body fat, lean mass, and insulin resistance were assessed using homeostasis model assessment (HOMA). After adjustment for confounders and at a given body fat, South Asian men had less lean mass than Aboriginal [3.42 kg less; 95% confidence interval (CI) = 1.55-5.29], Chinese (3.01 kg less; 95% CI = 1.33-4.70), and European (3.57 kg less; 95% CI = 1.82-5.33) men, whereas South Asian women had less lean mass than Aboriginal (1.98 kg less; 95% CI = 0.45-3.50), Chinese (2.24 kg less; 95% CI = 0.81-3.68), and European (2.97 kg less; 95% CI = 1.67-4.27) women. In adjusted models, F:LM was higher in South Asian compared with Chinese and European men and higher in South Asian compared with Aboriginal, Chinese, and European women (P < 0.01 for all). Insulin and HOMA were greatest in South Asians after adjustment; however, these differences were no longer apparent when F:LM was considered. South Asians have a phenotype of high fat mass and low lean mass, which may account for greater levels of insulin and HOMA compared with other ethnic groups.
    The Journal of clinical endocrinology and metabolism 10/2009; 94(12):4696-702. · 6.50 Impact Factor
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    Article: Ezetimibe is effective when added to maximally tolerated lipid lowering therapy in patients with HIV.
    Matthew T Bennett, Kevin W Johns, Gregory P Bondy
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    ABSTRACT: To determine the efficacy and safety of adding ezetimibe to maximally tolerated lipid lowering therapy in patients with HIV dyslipidemia. Retrospective analysis of lipid parameters was conducted for 33 patients with HIV who had been prescribed ezetimibe 10 mg per day. Mean total cholesterol was reduced 21% (p < 0.001). Mean LDL was reduced 35% (p < 0.001). Mean HDL increased 8% (p = 0.038). Mean triglyceride was reduced 34% (p = 0.006). Mean Apolipoprotein B100 was reduced 33% (p = 0.043). No adverse events occurred. Ezetimibe appears safe and effective in patients with HIV when added to maximally tolerated doses of lipid lowering therapy.
    Lipids in Health and Disease 01/2007; 6:15. · 2.17 Impact Factor
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    Article: Are HIV positive patients resistant to statin therapy?
    Kevin W Johns, Matthew T Bennett, Gregory P Bondy
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    ABSTRACT: Patients with HIV are subject to development of HIV metabolic syndrome characterized by dyslipidemia, lipodystrophy and insulin resistance secondary to highly active antiretroviral therapy (HAART). Rosuvastatin is a highly potent HMG-CoA reductase inhibitor. Rosuvastatin is effective at lowering LDL and poses a low risk for drug-drug interaction as it does not share the same metabolic pathway as HAART drugs. This study sought to determine the efficacy of rosuvastatin on lipid parameters in HIV positive patients with HIV metabolic syndrome. Mean TC decreased from 6.54 to 4.89 mmol/L (25.0% reduction, p < 0.001). Mean LDL-C decreased from 3.39 to 2.24 mmol/L (30.8% reduction, p < 0.001). Mean HDL rose from 1.04 to 1.06 mmol/L (2.0% increase, p = ns). Mean triglycerides decreased from 5.26 to 3.68 mmol/L (30.1% reduction, p < 0.001). Secondary analysis examining the effectiveness of rosuvastatin monotherapy (n = 70) vs. rosuvastatin plus fenofibrate (n = 43) showed an improvement of 21.3% in TG and a decrease of 4.1% in HDL-C in the monotherapy group. The rosuvastatin plus fenofibrate showed a greater drop in triglycerides (45.3%, p < 0.001) and an increase in HDL of 7.6% (p = 0.08). This study found that rosuvastatin is effective at improving potentially atherogenic lipid parameters in HIV-positive patients. The lipid changes we observed were of a smaller magnitude compared to non-HIV subjects. Our results are further supported by a small, pilot trial examining rosuvastatin effectiveness in HIV who reported similar median changes from baseline of -21.7% (TC), -22.4% (LDL-C), -30.1% (TG) with the exception of a 28.5% median increase in HDL. In light of the results revealed by this pilot study, clinicians may want to consider a possible resistance to statin therapy when treating patients with HIV metabolic syndrome.
    Lipids in Health and Disease 01/2007; 6:27. · 2.17 Impact Factor
  • Article: Estrogen replacement stimulates fatty acid oxidation and impairs post-ischemic recovery of hearts from ovariectomized female rats.
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    ABSTRACT: Women less than 50 years of age, the majority of whom are likely premenopausal and exposed to estrogen, are at greater risk of a poor short-term recovery after myocardial ischemia than men and older women. Since estrogen enhances non-cardiac lipid utilization and increased lipid utilization is associated with poor post-ischemic heart function, we determined the effect of estrogen replacement on post-ischemic myocardial function and fatty acid oxidation. Female Sprague-Dawley rats, either intact (n = 15) or ovariectomized and treated with 17beta-estradiol (0.1 mg x kg(-1) x day(-1), s.c., n = 14) or corn oil vehicle (n = 16) for 5 weeks, were compared. Function and fatty acid oxidation of isolated working hearts perfused with 1.2 mM [9,10-3H]palmitate, 5.5 mM glucose, 0.5 mM lactate, and 100 mU/L insulin were measured before and after global no-flow ischemia. Only 36% of hearts from estrogen-treated rats recovered after ischemia compared with 56% from vehicle-treated rats (p > 0.05, not significant), while 93% of hearts from intact rats recovered (p < 0.05). Relative to pre-ischemic values, post-ischemic function of estrogen-treated hearts (26.3 +/- 10.1%) was significantly lower than vehicle-treated hearts (53.4 +/- 11.8%, p < 0.05) and hearts from intact rats (81.9 +/- 7.0%, p < 0.05). Following ischemia, fatty acid oxidation was greater in estrogen-treated hearts than in the other groups. Thus, estrogen replacement stimulates fatty acid oxidation and impairs post-ischemic recovery of isolated working hearts from ovariectomized female rats.
    Canadian Journal of Physiology and Pharmacology 11/2002; 80(10):1001-7. · 1.95 Impact Factor
  • Article: Pyruvate dehydrogenase and the regulation of glucose oxidation in hypertrophied rat hearts.
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    ABSTRACT: Coupling of glucose oxidation to glycolysis is lower in hypertrophied than in non-hypertrophied hearts, contributing to the compromised mechanical performance of hypertrophied hearts. Here, we describe studies to test the hypothesis that low coupling of glucose oxidation to glycolysis in hypertrophied hearts is due to reduced activity and/or expression of the pyruvate dehydrogenase complex (PDC). We examined the effects of dichloroacetate (DCA), an inhibitor of PDC kinase, and of alterations in exogenous palmitate supply on coupling of glucose oxidation to glycolysis in isolated working hypertrophied and control hearts from aortic-constricted and sham-operated male Sprague-Dawley rats. It was anticipated that the addition of DCA or the absence of palmitate would promote PDC activation and consequently normalize coupling between glycolysis and glucose oxidation in hypertrophied hearts if our hypothesis was correct. Addition of DCA or removal of palmitate improved coupling of glucose oxidation to glycolysis in control and hypertrophied hearts. However, coupling remained substantially lower in hypertrophied hearts. PDC activity in extracts of hypertrophied hearts was similar to or higher than in extracts of control hearts under all perfusion conditions. No differences were observed between hypertrophied and control hearts with respect to expression of PDC, PDC kinase, or PDC phosphatase. Low coupling of glucose oxidation to glycolysis in hypertrophied hearts is not due to a reduction in PDC activity or subunit expression indicating that other mechanism(s) are responsible.
    Cardiovascular Research 04/2002; 53(4):841-51. · 6.06 Impact Factor
  • Article: Regression of Cardiac Hypertrophy Normalizes Glucose Metabolism and Left Ventricular Function During Reperfusion
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    ABSTRACT: It is not yet known if the alterations in myocardial glucose metabolism and the exaggerated left ventricular dysfunction that occur during reperfusion in hypertrophied hearts are reversible. Thus, we studied isolated working hearts from aortic-banded (n=29) and sham-operated control (n=32) male Sprague–Dawley rats with or without enalapril maleate treatment (25.6±0.8 mg/kg per day, p.o.) to determine the effect of regression of cardiac hypertrophy on myocardial glucose metabolism and post-ischemic heart function. Hearts were perfused with buffer containing 1.2 mmpalmitate, 11 mm[5-3H]/[U-14C]-glucose, 0.5 mmlactate and 100μU/ml insulin. Glucose metabolism [rates of glycolysis (3H2O production) and rates of oxidation (14CO2production) of exogenous glucose] and heart function (heart rate×peak systolic pressure) were measured during 30 min pre-ischemic perfusion and 60 min of reperfusion following 20 min of global, no-flow ischemia. Hearts from untreated aortic-banded rats were hypertrophied, being 27.6±1.8% larger than hearts from untreated control rats. Enalapril treatment caused regression of cardiac hypertrophy that normalized heart weight in aortic-banded rats. Rates of glycolysis of exogenous glucose in hearts from untreated aortic-banded rats were accelerated compared to rates in hearts from untreated control rats during pre-ischemic perfusion (4391±97v2652±69 nmol glucose/min per g dry wt, respectively,P<0.05) and reperfusion (2402±58v1597±88 nmol glucose/min per g dry wt, respectively,P<0.05). In contrast, rates of glycolysis of exogenous glucose in hearts from enalapril-treated aortic-banded rats were normalized before and after ischemia. Rates of glycolysis of exogenous glucose in hearts of control rats were not affected by enalapril treatment. Oxidation of exogenous glucose was not different among groups either before or after ischemia. Function of hearts from untreated aortic-banded rats at the end of reperfusion was significantly less than that of hearts from untreated control rats (23.9±2.6v32.2±0.7 mmHg×beats per min/1000, respectively,P<0.05). As with myocardial glucose metabolism, function of hearts from aortic-banded rats treated with enalapril was normalized during reperfusion. Thus, pharmacologically induced regression of pressure-overload cardiac hypertrophy normalizes glucose metabolism as well as left ventricular function during reperfusion.
    Journal of Molecular and Cellular Cardiology 03/1997; · 5.17 Impact Factor
  • Article: Prevalence of bone mineral density abnormalities and related risk factors in an ambulatory HIV clinic population.
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    ABSTRACT: Bone mineral density (BMD) abnormalities are observed frequently among human immunodeficiency virus (HIV)-infected patients. Risk factors for reduced BMD in the setting of HIV have been previously studied, but detailed antiretroviral treatment history is often not available. A cross-sectional observational study was conducted between 2005 and 2007 among unselected HIV-infected adults attending an ambulatory urban HIV clinic. Dual-energy X-ray absorptiometry (DXA) scans of lumbar spine and femoral neck, full laboratory profile, detailed questionnaire, and antiretroviral history were obtained. Univariate and multivariate logistic regression analyses were performed to investigate factors associated with BMD below the expected range for age. Two hundred ninety patients completed the study: 80% Caucasians, 89% males, with median age of 49 yr. Low BMD as assessed by Z-score was present in 19.7% of the patients. By multivariate analysis, only lower body mass index (BMI) was an independent risk factor for low BMD. Cumulative exposure to protease inhibitors, non-nucleosides, and individual nucleoside and nucleotide analogs were not independently associated with low BMD. In conclusion, a 19.7% prevalence of abnormal BMD by DXA scan was identified in an unselected group of HIV-infected adults. Lower BMI was independently associated with low BMD. No correlation was found between abnormal BMD and cumulative exposure to any antiretroviral agents.
    Journal of Clinical Densitometry 13(4):456-61. · 1.29 Impact Factor