Showing papers by "Barbara A. Gower published in 2002"
TL;DR: The results of this study suggest that greater AIR(g) among AA is due to both greater insulin secretion and lesser hepatic insulin extraction, and that AIR( g) above that predicted based on lower S(i) isdue to greater insulin gland secretion.
Abstract: Relative to Caucasians (C), African-American (AA) children and adults have lower indices of insulin sensitivity (Si) and a higher acute insulin response to glucose (AIRg). Among AA children, AIRg is greater than that which would be predicted based on lower Si. The objectives of the present study were 1) to determine whether insulin secretory parameters differ in AA vs. C children and adolescents using C-peptide modeling, 2) to determine whether hepatic insulin extraction differs with ethnicity/race using the C-peptide to insulin molar ratio, and 3) to determine whether the relatively greater AIRg among African-Americans is due to greater insulin secretion or lesser clearance. Subjects (n 76) were AA and C children (mean age, 11 yr). A 3-h tolbutamide-modified iv glucose tolerance test and minimal modeling were used to determine Si and AIRg. First phase C-peptide/insulin secretion and basal, first, and second phase -cell sensitivity to glucose were determined using C-peptide modeling with standard kinetic parameters developed in adults. The incremental C-peptide to insulin molar ratio over the 3-h test period, an index of hepatic insulin extraction, was calculated with the trapezoidal method. Si was lower and AIRg was higher in AA vs. C children. First phase C-peptide/insulin secretion and first phase -cell sensitivity to glucose were approximately 2-fold greater in AA vs. C children (P < 0.001); there were no between-group differences in basal or second phase -cell sensitivity to glucose. Hepatic insulin extraction was lower in AA vs. C (3.77 1.78% vs. 5.99 2.18%; P < 0.001). Multiple linear regression modeling indicated that first phase C-peptide/insulin secretion and hepatic insulin extraction contributed independently to AIRg; however, it was only first phase C-peptide/insulin secretion that explained the significant independent contribution of ethnicity/race to AIRg after adjusting for Si. The results of this study suggest that greater AIRg among AA is due to both greater insulin secretion and lesser hepatic insulin extraction, and that AIRg above that predicted based on lower Si is due to greater insulin secretion. The insulin secretion data await verification that the kinetic parameters used apply to children and AA. (J Clin Endocrinol Metab 87: 2218 –2224, 2002)
101 citations
TL;DR: It is suggested that in postmenopausal women, VATM is uniquely related to Si, and HRT affects the relationship between VATM and Si and between lean body mass and Si.
Abstract: Objective: To examine cross-sectionally the influence of hormone replacement therapy (HRT) on the relationship between body composition and insulin sensitivity (Si).
Research Methods and Procedures: Subjects were 57 early postmenopausal white women, 33 receiving HRT and 24 controls. Body composition was estimated using DXA and computed tomography scans at the abdomen and mid-thigh. Si was assessed by a frequently sampled intravenous glucose tolerance test with minimal model analysis.
Results: Compared with nonusers, HRT users had lower visceral adipose tissue, fasting serum glucose, and fasting insulin. Total body fat and unadjusted Si did not differ between groups. Visceral adipose tissue mass (VATM) was the only body-fat compartment significantly associated with Si (r2 = 0.43, p < 0.0001) in a model including total-body fat, upper-trunk fat, subcutaneous abdominal fat mass, leg fat, and mid-thigh low-density lean tissue. Lean body mass was positively correlated with Si among HRT users and tended to be negatively correlated among nonusers. HRT status also affected the relationship between VATM and Si such that, relative to nonusers, HRT users had lower Si across lower VATM levels, but higher Si across higher VATM.
Discussion: These results suggest that in postmenopausal women, VATM is uniquely related to Si. HRT affects the relationship between VATM and Si and between lean body mass and Si. These interactions should be considered in future studies.
97 citations
TL;DR: The relationship between insulin sensitivity and systolic blood pressure is evident early in life, and black ethnicity and low insulin sensitivity contribute independently to higher blood pressure in children.
Abstract: Although insulin sensitivity is correlated with high blood pressure in adults, it is unclear whether such a relationship exists in children across ethnic groups. Therefore, the aims of the study were to establish (1) if body composition and insulin sensitivity were related to blood pressure in children, and (2) if any differences in blood pressure between white and black children were explained by body composition and/or insulin sensitivity. Insulin sensitivity and the acute insulin response were established by the minimal model and body composition by dual-energy X-ray absorptiometry. Blood pressure was recorded in the supine position. Body composition, fasting insulin ( P P P P P =0.01) and diastolic (59±7.0 versus 54±8.0 mm Hg, P
76 citations
TL;DR: With weight loss, moderately overweight African American and white women experienced significant improvements in S(i) and lipids, and the beneficial effects of weight loss did not differ with race and could not be attributed to a specific body fat depot.
69 citations
TL;DR: Growth-related increases in abdominal fat, particularly subcutaneous abdominalFat, may contribute to accelerating increases in FI, but have no effect on SI; however, sub cutaneous abdominal fat may be more predictive of the rate of change of FI than visceral or total fat.
Abstract: HUANG, TERRY T.-K., MARIA S. JOHNSON, BARBARA A. GOWER, AND MICHAEL I. GORAN. Effect of changes in fat distribution on the rates of change of insulin response in children. Obes Res. 2002;10: 978 –984. Objective: To develop mixed models for examining longitudinal associations between rates of change in visceral, subcutaneous abdominal, and total body fat with rates of change in fasting insulin (FI) and insulin sensitivity (SI) over 3 years in children. Research Methods and Procedures: Seventy-seven children (mean age, 8.3 years at baseline) from Birmingham, Alabama, with three or more annual measures of FI and SI were included. Abdominal fat was measured by computed tomography, and total body fat and lean tissue mass were measured by DXA. Mixed models examined the longitudinal associations between the baseline level/rate of change of different fat compartments and the rate of change in FI or SI. Results: An annual increase of 5% in FI was associated with 1c m 2 /yr of visceral fat gain per year (p 0.05), independent of subcutaneous abdominal fat. A 1-cm 2 difference in initial subcutaneous abdominal fat was associated with an 0.2% increase per year in FI (p 0.02), independent of visceral fat. None of the rates of change in any of the fat measures was associated with the rate of change of SI. Discussion: The rate of change in visceral fat was positively associated with the rate of change in FI, independent of increasing subcutaneous abdominal fat; however, subcutaneous abdominal fat may be more predictive of the rate of change of FI than visceral or total fat. Therefore, growthrelated increases in abdominal fat, particularly subcutaneous abdominal fat, may contribute to accelerating increases in FI, but have no effect on SI.
34 citations
TL;DR: Despite obese mice having an excess of fat available for mitochondrial beta-oxidation in liver, overall energy balance appeared to dictate that the net liver FAO remained at control levels.
32 citations
TL;DR: It is suggested that, although E(2) is likely to suppress lipid oxidation and promote TG synthesis, these effects are not manifested in a relative increase in carcass adiposity after 18 days of treatment, at least under conditions of negative energy balance.
Abstract: GOWER, BARBARA A., TIM R. NAGY, MATTHEW L. BLAYLOCK, CHENXI WANG, AND LARA NYMAN. Estradiol may limit lipid oxidation via Cpt 1 expression and hormonal mechanisms. Obes Res. 2002;10:167–172. Objective: Evidence indicates that estrogen depresses hepatic lipid oxidation. We tested the hypothesis that estradiol (E2) treatment depresses transcription of carnitine palmitoyltransferase-1 (Cpt 1) mRNA and increases adiposity. Research Methods and Procedures: Six ovariectomized female rats were given a subcutaneous pellet of E2 (5 mg/d), and six were given placebo. Rats were pair-fed by group for 18 days. Body composition was assessed chemically: mRNA for liver Cpt 1, adipose tissue uncoupling protein-2 (Ucp 2), and quadriceps Ucp 3 by Northern analysis; serum glucose, triglycerides (TGs), and free fatty acids by standard techniques; and serum insulin and glucagon by radioimmunoassay. Results: E2-treated rats lost more weight than placebotreated rats (37.3 6.0 vs. 16.2 2.6 g, p 0.01), but did not differ in final carcass composition (adjusted for eviscerated body mass). E2-treated rats had lower liver Cpt 1 (p 0.001) and skeletal muscle Ucp 3 (p 0.05) mRNA and lower concentrations of glucose, glucagon, and free fatty acids (p 0.05). E2-treated rats tended to have higher insulin (p 0.067) and TG (p 0.097). TG tended to be correlated with Cpt 1 mRNA (r 0.56 and p 0.07). Discussion: These results suggest that, although E2 is likely to suppress lipid oxidation and promote TG synthesis, these effects are not manifested in a relative increase in carcass adiposity after 18 days of treatment, at least under conditions of negative energy balance. The possible role of E 2 mediated changes in insulin and glucagon secretion on hepatic substrate metabolism warrants further study.
26 citations