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Biomedical subjects

A D Karelis

Publications and source records attributed to A D Karelis.

7 recordsLinked to original sources
PubMed2006

Lifestyle behaviours and components of energy balance as independent predictors of ghrelin and adiponectin in young non-obese women.

AIM: Dysregulation of the normal levels of ghrelin, leptin and adiponectin in young non-obese subjects could promote food intake, diabetes and cardiovascular disease in later stages of life. Little information is available on how plasmatic concentrations of these hormones may be influenced by eating habits and/or components of energy balance in a young population, which if known, could facilitate their voluntary regulation. METHODS: In this cross-sectional study we examined the predictors of fasting plasma ghrelin, adiponectin and leptin in a population of well-characterized young non-obese women (N = 63). Energy intake was assessed by 24-hour dietary recall, resting metabolic rate (RMR) by indirect calorimetry, physical activity energy expenditure (PAEE) by tri-axial accelerometer, physical fitness by VO(2 peak), and eating behaviors by self administrated questionnaire. RESULTS: Lower RMR and higher HDL-cholesterol were independent predictors of higher plasma ghrelin explaining 17.6% of its variation even after correcting for BMI. Higher total or central fat mass was the only predictor of higher plasma leptin, and no other variable added any power to the prediction equation. Finally, higher energy intake and waist circumference and lower PAEE predicted lower plasma adiponectin in young non-obese women, explaining 43% of the variation in its concentrations even after correcting for total or central fat mass. CONCLUSION: Components of the energy balance (ie: energy intake and/or expenditure) influence adiponectin and ghrelin circulating levels. That is, higher energy intake and lower physical activity independently predict lower adiponectin concentrations, whereas lower resting metabolic rate independently predicts higher ghrelin levels in young non-obese women. Prospective studies are needed to examine whether circulating concentrations of ghrelin and adiponectin can be voluntarily regulated by lifestyle interventions.

Adiponectin↗
PubMed2006

Surrogate indexes vs. euglycaemic-hyperinsulinemic clamp as an indicator of insulin resistance and cardiovascular risk factors in overweight and obese postmenopausal women.

BACKGROUND: There is considerable interest in validating the most convenient method to estimate insulin sensitivity in clinical research protocols that could best indicate cardiovascular risk factors. To address this issue we examined the interrelationships of several cardiovascular risk factors with surrogate indexes such as fasting insulin, the homeostasis model assessment (HOMA), the quantitative insulin sensitivity check index (QUICKI) and the revised QUICKI vs the euglycaemic-hyperinsulinemic (EH) clamp in a non-diabetic overweight or obese postmenopausal female population. DESIGN: Cross-sectional study involving 88 obese postmenopausal women (age: 57.5+/-5.0 yrs; body mass index: 32.52+/-4.4 kg/m2; percent body fat: 46.35+/-4.9%). METHODS: Insulin sensitivity was determined by the EH clamp technique as well as by surrogate indexes such as fasting insulin, HOMA, log HOMA, QUICKI and revised QUICKI. Body composition and body fat distribution were measured using dual energy x-ray absorptiometry and computed tomography, respectively. RESULTS: Correlations between insulin resistance indexes (fasting insulin, revised QUICKI, QUICKI, log HOMA, HOMA) vs glucose disposal were similar (range of r's=0.40 to 0.49), suggesting that no index was superior to another with respect to its relationship with the EH clamp. Correlations between the insulin resistance indexes with plasma lipids were comparable among all indexes, however, systolic blood pressure, visceral fat and C-reactive protein were moderately superior with index vs the EH clamp. CONCLUSION: Surrogate measures of insulin resistance, in particular fasting insulin, are simple tools appropriate for epidemiological studies that can be used as substitutes for the EH clamp to estimate glucose disposal and cardiovascular risk factors in overweight and obese postmenopausal women.

Adipose Tissue↗
PubMed2006

Degradation in insulin sensitivity with increasing severity of the metabolic syndrome in obese postmenopausal women.

AIM: We investigated the relationship between insulin sensitivity and the graded increase in the number of features of the metabolic syndrome in a cross-sectional sample of obese postmenopausal women. We hypothesized that insulin sensitivity would deteriorate with an increased number of metabolic syndrome phenotypes. METHODS: Insulin sensitivity was measured in 75 obese postmenopausal women (age: 57.3 +/- 5.3 years; BMI: 32.8 +/- 4.5 kg/m2) by using both the hyperinsulinaemic-euglycaemic clamp and the homeostasis model assessment (HOMA-IR). Features of the metabolic syndrome included visceral fat (>130 cm2), HDL-cholesterol (<1.29 mmol/l), fasting triglycerides (> or =1.7 mmol/l), blood pressure (> or =130/> or =85 mmHg) and fasting glucose (> or =6.1 mmol/l). Participants were classified into three categories based on the presence of metabolic syndrome phenotypes: 0-1 vs. 2 vs. > or =3 features of the metabolic syndrome. RESULTS: We found that insulin sensitivity decreased in a graded fashion (12.19 +/- 3.2 vs. 11.80 +/- 2.3 vs. 9.29 +/- 2.6 mg/min/FFM) and HOMA-IR increased in a similar manner (2.95 +/- 1.1 vs. 3.28 +/- 1.3 vs. 4.65 +/- 2.2), as the number of features of the metabolic syndrome increased from 0-1 to > or =3. When insulin sensitivity was statistically adjusted for visceral fat (as measured by computed tomography) and plasma triglycerides, the differences among groups were abolished. CONCLUSIONS: These findings suggest that a decreased insulin sensitivity is associated with increased features of the metabolic syndrome in obese postmenopausal women and that visceral fat as well as plasma triglyceride accumulation might be potential mediators of this relationship.

Adipose Tissue↗
PubMed2004

Can we identify metabolically healthy but obese individuals (MHO)?

OBJECTIVES: A unique subset of obese individuals termed, Metabolically Healthy but Obese (MHO), has been described in the literature. However, there is no agreed upon method to identify MHO individuals for research protocols or in clinical practice. Therefore, we examined a large cohort of obese older women to attempt to develop a first set of clinical markers that may identify MHO individuals. METHODS: We studied 154 obese postmenopausal women (age: 57.0 +/- 5.3 years and BMI: 34.3 +/- 5.5 kg/m2). Selection criteria for MHO individuals were partially based on the National Cholesterol Education Program's Adult Treatment Panel III report (ATP III) for lipid profiles (triglycerides: < or =1.7 mmol/l, total cholesterol: < or =5.2 mmol/l, HDL-cholesterol: > or =1.3 mmol/l and LDL-cholesterol: < or =2.6 mmol/l) and from the study of Brochu et al. (2001) for insulin sensitivity (HOMA<=1.95). When 4 out of 5 criteria are met, we suggest that a diagnosis of the MHO individual could be made. RESULTS: Based on the proposed criteria, 19 out of 154 (12.3%) postmenopausal women subjects were identified as MHO. By design, MHO individuals showed a favourable lipid profile and higher insulin sensitivity values. CONCLUSION: We suggest a potential new set of clinical markers to identify MHO individuals. Identifying MHO individuals could have important implications for therapeutic medical decision making, subject characterization in research protocols and in medical education.

Blood Pressure↗