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Biomedical subjects

R S Weinstock

Publications and source records attributed to R S Weinstock.

At least 19 recordsLinked to original sources
PubMed2004

Exercise is required for visceral fat loss in postmenopausal women with type 2 diabetes.

This study examined the effects of aerobic exercise without weight loss, a hypocaloric high monounsaturated fat diet, and diet plus exercise (D+E) on total abdominal and visceral fat loss in obese postmenopausal women with type 2 diabetes. Thirty-three postmenopausal women (body mass index, 34.6 +/- 1.9 kg/m(2)) were assigned to one of three interventions: a hypocaloric high monounsaturated fat diet alone, exercise alone (EX), and D+E for 14 wk. Aerobic capacity, body composition, abdominal fat distribution (magnetic resonance imaging), glucose tolerance, and insulin sensitivity were measured pre- and postintervention. Body weight ( approximately 4.5 kg) and percent body fat ( approximately 5%) were decreased (P < 0.05) with the D and D+E intervention, whereas only percent body fat ( approximately 2.3%) decreased with EX. Total abdominal fat and sc adipose tissue (SAT) were reduced with the D and D+E interventions (P < 0.05), whereas visceral adipose tissue (VAT) decreased with the D+E and EX intervention, but not with the D intervention. EX resulted in a reduction in total abdominal fat, VAT, and SAT (P < 0.05) despite the lack of weight loss. The reductions in total abdominal fat and SAT explained 32.7% and 9.7%, respectively, of the variability in the changes in fasting glucose levels, whereas the reductions in VAT explained 15.9% of the changes in fasting insulin levels (P < 0.05). In conclusion, modest weight loss, through either D or D+E, resulted in similar improvements in total abdominal fat, SAT, and glycemic status in postmenopausal women with type 2 diabetes; however, the addition of exercise to diet is necessary for VAT loss. These data demonstrate the importance of exercise in the treatment of women with type 2 diabetes.

Adipose Tissue↗
PubMed2004

Influence of resistance exercise training on glucose control in women with type 2 diabetes.

The objective of the study was to evaluate the effects of acute and chronic resistance training on glucose and insulin responses to a glucose load in women with type 2 diabetes. Subjects consisted of type 2 diabetic women (n = 7) and age-matched controls (n = 8) with normal glucose tolerance. All subjects participated in 3 oral glucose tolerance tests: pretraining, 12 to 24 hours after the first exercise session (acute) and 60 to 72 hours after the final training session (chronic). Exercise training consisted of a whole body resistance exercise program using weight-lifting machines 3 days per week for 6 weeks. Resistance training was effective in increasing strength of all muscle groups in all subjects. Integrated glucose concentration expressed as area under the curve (AUC) was 3,355.0 +/- 324.6 mmol/L. min pretraining, improved significantly (P <.01) after the acute bout of exercise (2,868 +/- 324.0 mmol/L. min), but was not improved with chronic training (3,206.0 +/- 337.0 mmol/L. min) in diabetic subjects. A similar pattern of significance was observed with peak glucose concentration (pre: 20.2 +/-1.4 mmol/L; acute: 17.2 +/- 1.7 mmol/L; chronic: 19.9 +/- 1.7 mmol/L). There were no significant changes in insulin concentrations after any exercise bout in the diabetic subjects. There were no changes in glucose or insulin levels in control subjects. An acute bout of resistance exercise was effective in improving integrated glucose concentration, including reducing peak glucose concentrations in women with type 2 diabetes, but not age-matched controls. There were no significant changes in insulin concentrations for either group. Resistance exercise offers an alternative to aerobic exercise for improving glucose control in diabetic patients. To realize optimal glucose control benefits, individuals must follow a regular schedule that includes daily exercise.

Adult↗
PubMed2001

Resting leptin responses to acute and chronic resistance training in type 2 diabetic men and women.

PURPOSE: To evaluate the plasma leptin levels approximately 24 h post-exercise in control and type 2 diabetic subjects and to establish if observed changes in leptin concentrations were acute or chronic effects of a resistance training program. METHODS: Thirty men and women (17 controls and 13 type 2, obese diabetics, age 40-55 y) had resting blood samples drawn at 08:00 h (12 h postprandial) at the beginning of the study (pre-training), 24 h after a three repetition maximal weight lifting bout (acute) and 72 h after their last training bout of 6 weeks of resistance training (chronic). The two groups were not matched with respect to body mass index and the control subjects were not normal weight. Subjects weight-trained three times a week, for 6 weeks, for 1 h, training both the upper and lower body. RESULTS: Serum leptin concentrations were significantly higher in the type 2 diabetics than in the control group at pre-training (41.4+/-8.9 vs 11.4+/-3.0 ng/ml, P<0.05, respectively). Compared to pre-training, the leptin levels decreased significantly (P<0.01) after acute exercise in the diabetics but not in the control subjects (diabetics 30.9+/-7.1 vs controls 10.6+/-2.6 ng/ml). Approximately 72 h after 6 weeks of exercise training, the leptin concentrations were no longer lower than the pre-training values in either group (36.9+/-8.8 vs 11.9+/-8.8 ng/ml, respectively, P=NS). When leptin concentrations were log transformed and adjusted for fat mass there were still significant changes in leptin levels over time and between the control and diabetic group (P<0.05). CONCLUSIONS: The type 2 diabetics showed a significant 30% reduction in resting leptin levels 24 h after a single bout of resistance exercise. This was an acute response to resistance exercise and not a chronic training effect (no difference between pre-training and chronic). The decreased resting leptin concentrations approximately 24 h post-acute exercise may be due to reduced glucose availability to the adipose tissue, particularly in the diabetic subjects. There is no chronic effect of resistance exercise on leptin concentrations.

Adipose Tissue↗
PubMed2001

Abdominal fat distribution in pre- and postmenopausal women: The impact of physical activity, age, and menopausal status.

Age-related increases in total body fat have been reported, but the impact of menopause on abdominal fat distribution is still unclear. The purpose of this study was to determine the impact of menopausal status on abdominal fat distribution using magnetic resonance imaging (MRI). In addition, we investigated the influence of abdominal fat distribution on blood lipid profiles and leptin concentrations. Twenty-three premenopausal (PRE), 27 postmenopausal (POST), and 28 postmenopausal women on estrogen replacement therapy (ERT) had measurements of regional abdominal fat, blood lipids, and serum leptin concentrations. The women were matched for body mass index (BMI) and total body fat mass. Age and menopausal status were not found to be significant predictors of total abdominal fat, visceral fat, or subcutaneous fat, while physical activity was a significant predictor (P <.01) for total abdominal fat (R(2) =.16), visceral fat (R(2) =.32) and percent visceral fat (R(2) =.25). There was a trend for a greater visceral fat content in the POST women compared with the PRE women (2,495.0 +/- 228.4 v 1,770.4 +/- 240.8 cm(2), respectively, P =.06). The percent visceral abdominal fat was significantly lower (P <.05) in the premenopausal women than in either postmenopausal group (PRE, 23.2% +/- 1.7%; POST, 28.9% +/- 1.8%; ERT, 28.9% +/- 1.6%). Menopausal status and age did not influence any of the blood lipid values. Abdominal fat distribution was a significant predictor of cholesterol concentrations and the cholesterol/high-density lipoprotein-cholesterol (HDL-C) ratio, but only accounted for approximately 15% of the variability in these levels. Total body fat and physical activity accounted for 47% of the variability in leptin concentrations, while abdominal fat distribution, age, and menopausal status were not significant predictors. In conclusion, in early postmenopausal women, the level of physical activity accounts for the variability in abdominal fat distribution observed, while menopausal status and age do not play a significant role. ERT was not associated with additional benefits in abdominal fat distribution compared with postmenopausal women not on ERT or in the blood lipid profile in these women.

Abdomen↗
PubMed2001

The marital relationship and psychosocial adaptation and glycemic control of individuals with diabetes.

OBJECTIVE: To explore the relationship between marital relationship domains (i.e., intimacy and adjustment) and glycemic control and psychosocial adaptation to diabetes. RESEARCH DESIGN AND METHODS: A total of 78 insulin-treated adults with both type 1 and type 2 diabetes were assessed on a single occasion. They completed two marital quality measures (Spanier Dyadic Adjustment Scale and Personal Assessment of Intimacy in Relationships Scale) and four quality-of-life measures (Diabetes Quality of Life Scale, Medical Outcomes Study Health Survey, Problem Areas in Diabetes Scale, and Positive and Negative Affect Scale). Glycemic control was assessed by HbA(1c). Demographic data (age, sex, type and duration of diabetes, years married, other medical conditions, family history, disability, and years of education) were gathered from the chart and questionnaires. RESULTS: Concerning psychosocial adaptation, both of the marital quality measures were predictors of aspects of adaptation. Better marital satisfaction was related to higher levels of diabetes-related satisfaction and less impact, as well as less diabetes-related distress and better general quality of life. Higher levels of marital intimacy were related to better diabetes-specific and general quality of life. Concerning glycemic control, there was a nonsignificant trend for marital adjustment scores to relate to HbA(1c) (P = 0.0568). CONCLUSIONS: For insulin-treated adults with diabetes, quality of marriage is associated with adaptation to diabetes and other aspects of health-related quality of life. The suggestive finding that marital adjustment may relate to glycemic control warrants further study. Future work should also explore the impact of couples-focused interventions on adaptation, adherence, and glycemic control.

Adaptation, Psychological↗
PubMed1999

Impact of the work environment on glycemic control and adaptation to diabetes.

OBJECTIVE: To evaluate quantitatively whether the work environments of adults with diabetes relate to the adequacy of metabolic control and/or to the individual's adaptation to diabetes and to explore qualitatively the interactions between an individual's life at work and ways of coping with diabetes. RESEARCH DESIGN AND METHODS: A total of 129 insulin-requiring adults who were employed outside of the home were assessed on a single occasion. They completed two work system measures (The Work Environment Scale and The Work Apgar Scale) and two quality-of-life measures (The Diabetes Quality of Life Scale and The Appraisal of Diabetes Scale). Subjects also participated in a semi-structured interview concerning the interaction of work and diabetes. Glycemic control was assessed by using HbAlc results. Demographic data (age, sex, diabetes type, duration of diabetes, number of diabetes-related medical complications) were gathered from the charts. RESULTS: Concerning glycemic control, neither of the work system measures was a significant predictor of HbAlc. Concerning psychosocial adaptation, supervisor support was found to be a significant predictor of positive appraisal and diabetes-related satisfaction. Involvement and coworker cohesion also predicted aspects of diabetes-related quality of life. Interview themes showed that for a minority (18%), diabetes affected choice of work and that for a majority (60%), diabetes affected relationships at work and raised financial/job concerns (49%). Most adjust their diet, blood glucose testing, and exercise regimen through work-related modifications. CONCLUSIONS: For insulin-treated adults with diabetes, work system variables do not directly relate to glycemic control, but they do relate to psychosocial adaptation. Future work should examine further the specific aspects of the workplace that might affect adaptation, with the goal being to develop worksite interventions that target not only the employee with diabetes but also their supervisors and coworkers.

Adaptation, Physiological↗
PubMed1998

Translocation of PKC delta by insulin in a rat hepatoma cell line.

The aim of this study was to examine the effects of insulin and phorbol 12-myristate 13-acetate (PMA), an activator of classic and novel PKCs, on the translocation of PKC from cytosol to membrane in H4IIE (H4) rat hepatoma cells. Six PKC isoforms were expressed, including PKC-mu and PKC-lambda, identified for the first time in this hepatoma-cell line. Insulin induced translocation of PKC-delta from the cytosol to the membrane fraction as early as 15 min and maximally at 60 min with levels returning to that of controls by 180 min. Insulin also decreased levels of PKC-zeta in membranes at 5, 10, 15, and 30 min, but had no effect on cytosol levels. Ten minutes of PMA treatment translocated PKC-delta completely, and 24 h of PMA treatment downregulated PKC-delta. Neither acute nor chronic PMA had any effect on PKC-zeta. These studies establish the ability of both insulin and PMA to activate PKC-delta in H4 cells, and coupled with our previous work demonstrating a diminution of the effect of insulin on gene transcription in PKC downregulated cells, suggest that insulin may exert specific effects, in part, through a PKC-dependent pathway.

Animals↗
PubMed1998

Family environment, glycemic control, and the psychosocial adaptation of adults with diabetes.

OBJECTIVE: To evaluate whether the family system variables of adults with diabetes relate to the adequacy of metabolic control or the psychosocial adaptation to the illness. RESEARCH DESIGN AND METHODS: A total of 150 insulin-requiring adults were assessed on a single occasion. They completed two family system measures (the Family Environment Scale [FES] and the Diabetes Family Behavior Checklist [DFBC]), two quality-of-life measures (the Diabetes Quality of Life Scale and the Medical Outcomes Study Health Survey-36), and one measure of cognitive appraisal (the Appraisal of Diabetes Scale). Glycemic control was assessed using HbA1c results. Demographic data (age, sex, diabetes type, duration of diabetes, and number of diabetes-related medical complications) were gathered from the patients' charts. RESULTS: Concerning glycemic control, none of the family system measures were significant predictors of HbA1c. Older age and longer duration of diabetes predicted higher HbA1c values. For psychosocial adaptation, when family members behaved in ways that supported the diabetes care regimen (measured by the DFBC), the individual with diabetes was more satisfied with his or her adaptation to the illness and reported less interference in role function due to emotional problems. Family cohesion (measured by the FES) also related to better physical function. Women reported higher levels of diabetes satisfaction. The Appraisal of Diabetes Scale predicted glycemic control and psychosocial adaptation. CONCLUSIONS: For insulin-treated adults with diabetes, family system variables do not relate to glycemic control, but they do relate to psychosocial adaptation. Future work should explore the impact of family-centered interventions on adaptation, sex differences in adaptation, and the use of the Appraisal of Diabetes Scale as a first-line clinical screening tool.

Adaptation, Psychological↗
PubMed1997

Pioglitazone: in vitro effects on rat hepatoma cells and in vivo liver hypertrophy in KKAy mice.

Pioglitazone increases insulin sensitivity in vivo and in vitro. The effects of this agent on insulin-induced DNA synthesis and hepatic cell growth have not been determined. We examined the ability of pioglitazone to enhance basal and insulin-stimulated DNA synthesis in rat H4IIE (H4) hepatoma cells, and to alter liver weight and histology in diabetic KKAy mice. Treatment of H4 cells with increasing concentrations of pioglitazone for 30 h increased basal DNA synthesis 1.6- to 1.8-fold. With pioglitazone pretreatment and submaximal insulin concentrations, DNA synthesis was significantly increased from 2.1-fold (insulin 10(-12) mol/l alone) to 3.9-fold (insulin 10(-12) mol/l + pioglitazone 10(-6) mol/l). At maximal concentrations of insulin, the enhancement of DNA synthesis increased from 7.4-fold (insulin 10(-8) mol/l alone) to 16.2-fold (insulin 10(-8) mol/l + pioglitazone 10(-6) mol/l). Glyburide did not increase basal or insulin-stimulated DNA synthesis. In diabetic KKAy mice, serum glucose levels decreased and body weight, liver weight and liver weight as a percentage of body weight increased following pioglitazone treatment. Histological studies demonstrated marked hepatocyte distension. Our findings suggest that pioglitazone acts as an insulin sensitizer in rat hepatoma cells, increasing basal and insulin-stimulated DNA synthesis, and stimulating fat synthesis and liver hypertrophy in diabetic KKAy mice.

Animals↗
PubMed1995

Relation of weight loss to changes in serum lipids and lipoproteins in obese women.

Several reports have suggested that modest weight losses, as little as 10% of initial weight, are sufficient to control many of the health complications of obesity. This study examined the relation between changes in weight and those in serum lipids and lipoproteins in obese women who participated in a 48-wk weight-reduction study. Subjects were 66 obese women who were prescribed a 3870-kJ (925-kcal)/d diet for the first 16 wk and a balanced-deficit diet of 5029-6279 kJ (1200-1500 kcal)/d thereafter. Anthropometric measures were assessed at baseline and weeks 8, 24, and 48, as were serum triacylglycerols (triglycerides), total cholesterol, and low-density-lipoprotein- and high-density-lipoprotein-cholesterol concentrations. Weight decreased 11.1% during the first 8 wk, during which time triacylglycerols and total cholesterol fell 22.7% and 15.7%, respectively. Subjects lost an additional 4.7 kg (equal to a total reduction of 16.4%) between weeks 8 and 24 but triacylglycerols and total and low-density-lipoprotein cholesterol increased by 5.2%, 4.2%, and 4.5%, respectively during this time. Multiple-regression analyses showed that at no time did weight loss account for > 6% of the variance in the reductions in triacylglycerol and cholesterol concentrations. These findings indicate that modest weight losses are associated with significant improvements in serum lipids, but that factors including the energy and macronutrient content of the diet prescribed contribute significantly to the improvements observed.

Adult↗
PubMed1994

Synergistic induction of gene 33 expression by retinoic acid and insulin.

The expression of gene 33 in rat liver and hepatoma cells is regulated by multiple hormones and other bioactive agents. Previous studies have demonstrated a 15-fold increase in gene 33 mRNA after 1 h of insulin treatment. We demonstrate in this report that retinoic acid (RA) also controls the expression of this gene. Gene 33 mRNA levels are rapidly elevated by RA, with maximal accumulation (19-fold over control) attained after just 1 h of RA treatment. The transcription rate of gene 33 was increased by RA to a maximum level 6-fold greater than control values. Studies with inhibitors of RNA synthesis demonstrated no increase in the stability of gene 33 mRNA in response to RA or insulin. In addition, a synergistic induction of both gene 33 mRNA levels and the transcription rate of gene 33 was observed when both RA and insulin were added together. In the presence of both hormones, the transcription rate was induced almost 20-fold in 30 min, followed by a 49-fold increase in mRNA levels after 1 h. Thus, gene 33 represents the first example of a gene whose transcription rate is elevated directly by both insulin and RA, and synergistically elevated by treatment with both hormones together.

Animals↗
PubMed1994

Evidence for diverse roles of protein kinase-C in the inhibition of gene expression by insulin: the tyrosine aminotransferase, albumin, and phosphoenolpyruvate carboxykinase genes.

We have previously shown that insulin is less effective in inducing expression of several genes in H4 hepatoma cells with reduced functional protein kinase-C (PKC) activity. However, other reports suggest that insulin regulation of gene transcription is not PKC dependent. Insulin and phorbol 12-myristate 13-acetate (PMA) rapidly inhibit transcription of the tyrosine aminotransferase and albumin genes. Prolonged PMA pretreatment, to desensitize cells to PMA, resulted in a loss of insulin ability to inhibit albumin transcription. Insulin was still able to inhibit tyrosine aminotransferase transcription, but less than in non-PMA-pretreated cells, and there was also a slight decrease in the ability of insulin to inhibit phosphoenolpyruvate carboxykinase transcription. We previously demonstrated decreased responsiveness of PMA-induced gene expression in insulin-desensitized cells. In the present work, using insulin-desensitized H4 cells (insulin pretreatment for 24 h), subsequent treatment with PMA did not alter phosphoenolpyruvate carboxykinase transcription rates, whereas PMA did inhibit tyrosine aminotransferase transcription rates to an extent similar to observed in nonpretreated cells. Unexpectedly, there was a significant increase in albumin transcription after PMA addition to insulin-pretreated cells. These findings support our hypothesis that the role of PKC in the regulation of gene expression by insulin varies for different insulin-regulated genes.

Animals↗
PubMed1993

Olfactory dysfunction in diabetes mellitus.

Olfactory dysfunction has been reported in individuals with diabetes mellitus, but the etiology is unknown. Diabetes is often complicated by serious medical conditions which could be related to the development of decreased olfactory ability. Overall, our 111 subjects with diabetes showed deficiencies in their ability to identify odorants measured with the Odorant Confusion Matrix (mean = 67.8% correct). The presence of macrovascular disease was found to be associated with olfactory dysfunction. Glycemic control as well as the type and duration of diabetes were not related to olfactory ability. Also, there was no distinct association with the presence of neuropathy, retinopathy, nephropathy, hypertension, or impotence. Consistent with previous studies utilizing measures of odorant identification, performance decreased with increased age, females were somewhat superior to males, and smoking had a deleterious effect. Other nondiabetes-related medical conditions and medications had no apparent effect on the olfactory ability of our subjects. These results suggest that the sequelae associated with macrovascular disease, such as perhaps, ischemia, to the olfactory area, impact negatively on olfactory ability.

Adult↗
PubMed1993

Role of cytosolic calcium in regulation of cytoskeletal gene expression by insulin.

Insulin and calcium ionophores rapidly stimulated transcription of the cytoskeletal beta- and gamma-actin genes in serum-deprived rat H4-II-E hepatoma cells. The calcium ionophore A23187 (1 microM) stimulated transcription of the beta-actin gene by 7.3-, 5.4-, and 2.6-fold and the gamma-actin gene by 5.9-, 5.6-, and 2.6-fold at 15, 30, and 60 min, respectively. Ionomycin (1 microM) similarly increased beta- and gamma-actin transcription. Insulin stimulated beta-actin transcription 11.4-fold and gamma-actin 8.4-fold at 30 min. alpha-Tubulin transcription was induced by both insulin and calcium ionophores but to a lesser degree. The effects of A23187 or ionomycin together with insulin for 30 min were no greater than those of insulin alone. Insulin alone, however, did not significantly increase measurable intracellular calcium concentrations in fura-2-loaded cells. When cytosolic calcium was chelated using quin2 acetoxymethyl ester, the ability of A23187 to increase beta- and gamma-actin transcription was completely abolished, whereas insulin's ability to stimulate actin transcription was only partially inhibited. This suggests that the regulation of gene transcription by insulin may include calcium-dependent pathways but strongly implies that calcium-independent pathways are also utilized.

Actins↗
PubMed1992

Vanadate and insulin stimulate gene 33 expression.

Vanadate and insulin stimulated gene 33 expression in rat H4 hepatoma cells. Vanadate (10(-3) M) maximally increased gene 33 transcription 4-fold at 15 min. The maximal insulin induction (3-4-fold) was observed using 5 x 10(-9) M insulin for 30 min. Both vanadate and insulin increased cytoplasmic mRNA levels in a dose-dependent manner, with maximal effects observed by 60 min. These effects on gene 33 mRNA accumulation were greater than those on transcription. Vanadate (10(-3) M) maximally stimulated gene 33 mRNA levels 10-12-fold. The vanadate and insulin effects were not synergistic. Thus, high concentrations of vanadate regulate gene 33 expression in an insulin-like manner and, like insulin, vanadate probably controls transcriptional as well as post-transcriptional events.

Animals↗