OBJECTIVE -Glucagon-like peptide (GLP)-1 is a gut hormone that exerts incretin effects and suppresses food intake in humans, but its therapeutic use is limited due to its short half-life. This was a randomized, double-blind, parallel-group, placebo-controlled trial investigating the effect of the long-acting GLP-1 derivative liraglutide (NN2211) on glycemic control, body weight, body composition, and 24-h energy expenditure in obese subjects with type 2 diabetes.RESEARCH DESIGN AND METHODS -Thirty-three patients (mean Ϯ SD) aged 60.0 Ϯ 9.5 years, with HbA 1c 7.5 Ϯ 1.2% and BMI 36.6 Ϯ 4.1 kg/m 2 , were randomized to treatment with a single daily subcutaneous dose of 0.6 mg liraglutide (n ϭ 21) or placebo (n ϭ 12) for 8 weeks. In addition to weight and glycemic parameters, body composition was assessed by dual-energy X-ray absorptiometry (DEXA) scanning and 24-h energy expenditure in a respiratory chamber.RESULTS -After 8 weeks, liraglutide reduced fasting serum glucose (liraglutide, Ϫ1.90 mmol/l, and placebo, 0.27 mmol/l; P ϭ 0.002) and HbA 1c (liraglutide, Ϫ0.33%, and placebo, 0.47%; P ϭ 0.028) compared with placebo. No change in body weight was detected (liraglutide, Ϫ0.7 kg, and placebo, Ϫ0.9 kg; P ϭ 0.756). There was a nonsignificant trend toward a decrease in total fat mass (liraglutide, Ϫ0.98%, and placebo, Ϫ0.12%; P ϭ 0.088) and toward an increase in lean body mass (liraglutide, 1.02%, and placebo, 0.23%; P ϭ 0.118) in the liraglutide group compared with the placebo group. Twenty-four-hour energy expenditure was unaffected by the treatment (liraglutide, Ϫ12.6 kJ/h, and placebo, Ϫ13.7 kJ/h; P ϭ 0.799).CONCLUSIONS -Eight weeks of 0.6-mg liraglutide treatment significantly improved glycemic control without increasing weight in subjects with type 2 diabetes compared with those on placebo. No influence on 24-h energy expenditure was detected. Diabetes Care 27:1915-1921, 2004G lucagon-like peptide (GLP)-1 has several effects that make it a potential candidate molecule for the treatment of type 2 diabetes. GLP-1 is a peptide hormone secreted from the L-cells in the lower gut, i.e., the distal jejunum, ileum, and colon/rectum, in response to ingestion of carbohydrates, lipids, and mixed meals (1-3). GLP-1 stimulates postprandial insulin secretion and acts as an incretin hormone, thus potentiating glucose-stimulated insulin release. The incretin effect refers to the increased insulin response elicited by oral glucose compared with the response resulting from an isoglycemic intravenous infusion (4). In addition, GLP-1 has a suppressive effect on glucagon release and hepatic glucose output (5).Treatment of hyperglycemia in type 2 diabetic patients with GLP-1 has received much attention, but additional therapeutic indications could be envisioned. Within the last few years, the ability of GLP-1 to decrease appetite and energy intake has been established (6). A reduced food intake would support weight reduction attempts in patients with type 2 diabetes. The appetite-reducing effect might partly be related to the ability...
OBJECTIVE -The aim of this study was to determine whether overweight and obese individuals with type 2 diabetes have higher basal and 24-h energy expenditure compared with healthy control subjects before and after adjustment for body composition, spontaneous physical activity (SPA), sex, and age.RESEARCH DESIGN AND METHODS -Data from 31 subjects with type 2 diabetes and 61 nondiabetic control subjects were analyzed. The 24-h energy expenditure, basal metabolic rate (BMR), and sleeping energy expenditure (EE sleep ) between 1:00 A.M. and 6:00 A.M. were measured in whole-body respiratory chambers. Body composition was assessed by dual-energy X-ray absorptiometry (DXA).RESULTS -No significant differences in unadjusted EE sleep , BMR, and 24-h energy expenditure were observed between the type 2 diabetic group and the control group. After adjustment for fat-free mass (FFM), fat mass, SPA, sex, and age, EE sleep and BMR were, respectively, 7.7 and 6.9% higher in the type 2 diabetic group compared with the control group. This was equivalent to 144 Ϯ 40 kcal/day (P ϭ 0.001) and 139 Ϯ 61 kcal/day (P ϭ 0.026), respectively. Adjusted 24-h energy expenditure was 6.5% higher in the type 2 diabetic group compared with the nondiabetic control subjects (2,679 Ϯ 37 vs. 2,515 Ϯ 23 kcal/day, P ϭ 0.002). In multiple regression analyses, FFM, fat mass, SPA, and diabetes status were all significant determinants of EE sleep and 24-h energy expenditure, explaining 83 and 81% of the variation, respectively.CONCLUSIONS -This study confirms reports in Pima Indians that basal and 24-h energy expenditure adjusted for body composition, SPA, sex, and age are higher in individuals with type 2 diabetes compared with nondiabetic control subjects and may be even more pronounced in Caucasians. Diabetes Care 27:2416 -2421, 2004T he development of type 2 diabetes depends on both genetic susceptibility and environmental factors (1). An inappropriately high-energy intake and a sedentary lifestyle are wellknown risk factors for obesity, and there is solid evidence that excessive fat mass is the major cause of type 2 diabetes (2,3). Furthermore, large intervention trials have demonstrated that even a moderate, sustained weight loss in high-risk individuals can reduce the incidence of type 2 diabetes (4,5). However, genetic and disease-related differences in energy expenditure may also be important etiological determinants.A low resting energy expenditure (EE rest ) is a risk factor for weight gain (6). Paradoxically, cross-sectional studies have indicated an ϳ5% increased EE rest in Pima Indians with type 2 diabetes compared with nondiabetic individuals after adjustment for age and body composition (7-9). Other studies found a decreased thermogenic response to meals (10) and insulin/glucose clamp infusions among type 2 diabetic subjects compared with nondiabetic individuals (11). Thus, the integrated effect on total 24-h energy expenditure has been reported to be similar or only slightly elevated in Pima Indians with type 2 diabetes compared with nondia...
OBJECTIVE:To test the effect of low calorie diet (LCD) on body weight, lipid profile, and glycemic control in obese type 2 diabetes mellitus (DM) patients. DESIGN: Dietary intervention. SETTING: Department of Human Nutrition, Copenhagen. SUBJECTS: Outpatients: 11 type 2 DM patients (three males/eight females) (10 completed), four on oral hypoglycemic agents (OHA). Body mass index (BMI) 36.875.5 kg/m 2 and age 6275.7 y. INTERVENTIONS: In all, 8 weeks full meal-replacement diet: eight sachets of a nutrition powder (Nutrilett s , 850 kcal/day). Lipid profile assessed by NMR spectroscopy. RESULTS: Mean body weight fell by 10.9 kg (B11%, Po0.001). Fasting insulin, fasting blood glucose, hemoglobin A 1c , fasting plasma triglycerides, total cholesterol, and low-density lipoprotein (LDL) cholesterol fell significantly. There were large positive changes (statistically insignificant) in LDL subclass distribution and a similar shift in high-density lipoprotein subclass distribution. Medication was discontinued in all four subjects taking OHA for 2 weeks prior to the intervention and throughout the whole 8-week intervention period. CONCLUSION: LCD is effective in improving glycemic control and blood lipids through weight loss in overweight type 2 DM patients.
The present study demonstrated that ferulic acid from rye bran is bioavailable and that the urinary concentration of ferulic acid reflects the dietary intake of this hydroxycinnamic acid. Within the period of intervention, the elevated ferulic acid did not produce a measurable antioxidative effect on the subjects' LDL. It is suggested that the determination of ferulic acid in urine is a useful biomarker to assess the intake of ferulic acid from a regular diet.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.