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  • High multivitamin intake by Wistar rats during pregnancy results in increased food intake and components of the metabolic syndrome in male offspring. 18525008

    The effect of high multivitamin intake during pregnancy on the metabolic phenotype of rat offspring was investigated. Pregnant Wistar rats (n=10 per group) were fed the AIN-93G diet with the recommended vitamin (RV) content or a 10-fold increase [high vitamin (HV) content]. In experiment 1, male and female offspring were followed for 12 wk after weaning; in experiment 2, only males were followed for 28 wk. Body weight (BW) was measured weekly. Every 4 wk, after an overnight fast, food intake over 1 h was measured 30 min after a gavage of glucose or water. An oral glucose tolerance test was performed every 3-5 wk. Postweaning fasting glucose, insulin, ghrelin, glucagon-like peptide-1, and systolic blood pressure were measured. No difference in BW at birth or litter size was observed. Food intake was greater in males born to HV dams (P0.05), and at 28 wk after weaning, BW was 8% higher (P0.05) and fat pad mass was 27% higher (P0.05). Food intake reduction after the glucose preload was nearly twofold less in males born to HV dams at 12 wk after weaning (P0.05). Fasting glucose, insulin, and ghrelin were 11%, 62%, and 41% higher in males from HV dams at 14 wk after weaning (P0.05). Blood glucose response was 46% higher at 23 wk after weaning (P0.01), and systolic blood pressure was 16% higher at 28 wk after weaning (P0.05). In conclusion, high multivitamin intake during pregnancy programmed the male offspring for the development of the components of metabolic syndrome in adulthood, possibly by its effects on central mechanisms of food intake control.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Effective and safe gene-based delivery of GLP-1 using chitosanplasmid-DNA therapeutic nanocomplexes in an animal model of type 2 diabetes. 21412280

    Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates blood glucose level post-prandially. It has been proposed that GLP-1 can be used in type 2 diabetes (T2D) mellitus treatment because of its insulinotropic action. Despite its remarkable advantages, GLP-1 suffers the disadvantage of an extremely short half-life owing to its degradation by the dipeptidyl peptidase IV protease. One way of overcoming this drawback is GLP-1 gene delivery. Here we show effective and safe gene-based delivery of GLP-1 using chitosan/plasmid-DNA therapeutic nanocomplexes (TNCs) in Zucker diabetic fatty (ZDF) animal model of T2D. The expression plasmid fused the GLP-1 gene to a Furin cleavage site was driven by a cytomegalovirus promoter/enhancer. TNCs were prepared by mixing this plasmid with chitosans of specific molecular weight (MW), degree of deacetylation (DDA) and ratio of chitosan amine to DNA phosphate (N:P ratio). Animals injected with the TNC chitosan 92-10-5 (DDA-MW-N:P) showed GLP-1 plasma levels of about fivefold higher than that in non-treated animals and the insulinotropic effect of recombinant GLP-1 was shown by a threefold increase in plasma insulin concentration when compared with untreated animals. Intraperitoneal glucose tolerance tests revealed an efficacious decrease of blood glucose compared with controls for up to 24 days after treatment, where injections of this formulation allowed near-normalization of blood glucose level. TNCs composed of specific chitosans and GLP-1-expressing plasmid constructs showed an impressive ability to harness the profound therapeutic potential of GLP-1 for the treatment of T2D mellitus.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Engineered glucagon-like peptide-1-producing hepatocytes lower plasma glucose levels in mice. 19190262

    Glucagon-like peptide (GLP)-1 is an incretin hormone with well-characterized antidiabetic properties, including glucose-dependent stimulation of insulin secretion and enhancement of beta-cell mass. GLP-1 agonists have recently been developed and are now in clinical use for the treatment of type 2 diabetes. Rapid degradation of GLP-1 by enzymes including dipeptidyl-peptidase (DPP)-IV and neutral endopeptidase (NEP) 24.11, along with renal clearance, contribute to a short biological half-life, necessitating frequent injections to maintain therapeutic efficacy. Gene therapy may represent a promising alternative approach for achieving long-term increases in endogenous release of GLP-1. We have developed a novel strategy for glucose-regulated production of GLP-1 in hepatocytes by expressing a DPP-IV-resistant GLP-1 peptide in hepatocytes under control of the liver-type pyruvate kinase promoter. Adenoviral delivery of this construct to hepatocytes in vitro resulted in production and secretion of bioactive GLP-1 as measured by a luciferase-based bioassay developed to detect the NH(2)-terminally modified GLP-1 peptide engineered for this study. Transplantation of encapsulated hepatocytes into CD-1 mice resulted in an increase in plasma GLP-1 levels that was accompanied by a significant reduction in fasting plasma glucose levels. The results from this study demonstrate that a gene therapy approach designed to induce GLP-1 production in hepatocytes may represent a novel strategy for long-term secretion of bioactive GLP-1 for the treatment of type 2 diabetes.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Compensation for obesity-induced insulin resistance in dogs: assessment of the effects of leptin, adiponectin, and glucagon-like peptide-1 using path analysis. 21474268

    The hormonal mediators of obesity-induced insulin resistance and compensatory hyperinsulinemia in dogs have not been identified. Plasma samples were obtained after a 24-h fast from 104 client-owned lean, overweight, and obese dogs. Plasma glucose and insulin concentrations were used to calculate insulin sensitivity and β-cell function with the use of the homeostasis model assessment (HOMA(insulin sensitivity) and HOMA(β-cell function), respectively). Path analysis with multivariable linear regression was used to identify whether fasting plasma leptin, adiponectin, or glucagon-like peptide-1 concentrations were associated with adiposity, insulin sensitivity, and basal insulin secretion. None of the dogs were hyperglycemic. In the final path model, adiposity was positively associated with leptin (P < 0.01) and glucagon-like peptide-1 (P = 0.04) concentrations. No significant total effect of adiposity on adiponectin in dogs (P = 0.24) was observed. If there is a direct effect of leptin on adiponectin, then our results indicate that this is a positive relationship, which at least partly counters a negative direct relationship between adiposity and adiponectin. Fasting plasma leptin concentration was directly negatively associated with fasting insulin sensitivity (P = 0.01) and positively associated with β-cell function (P < 0.01), but no direct association was observed between adiponectin concentration and either insulin sensitivity or β-cell function (P = 0.42 and 0.11, respectively). We conclude that dogs compensate effectively for obesity-induced insulin resistance. Fasting plasma leptin concentrations appear to be associated with obesity-associated changes in insulin sensitivity and compensatory hyperinsulinemia in naturally occurring obese dogs. Adiponectin does not appear to be involved in the pathophysiology of obesity-associated changes in insulin sensitivity.Copyright © 2011 Elsevier Inc. All rights reserved.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • The effect of multidisciplinary lifestyle intervention on the pre- and postprandial plasma gut Peptide concentrations in children with obesity. 22363876

    Objective. This study aims to evaluate the effect of a multidisciplinary treatment of obesity on plasma concentrations of several gut hormones in fasting condition and in response to a mixed meal in children. Methods. Complete data were available from 36 obese children (age 13.3 ± 2.0 yr). At baseline and after the 3-month multidisciplinary treatment, fasting and postprandial blood samples were taken for glucose, insulin, ghrelin, peptide YY (PYY), and glucagon-like peptide 1 (GLP-1). Results. BMI-SDS was significantly reduced by multidisciplinary treatment (from 4.2 ± 0.7 to 4.0 ± 0.9, P < .01). The intervention significantly increased the area under the curve (AUC) of ghrelin (from 92.3 ± 18.3 to 97.9 ± 18.2 pg/L, P < .01), but no significant changes were found for PYY or GLP-1 concentrations (in fasting or postprandial condition). The insulin resistance index (HOMA-IR) remained unchanged as well. Conclusion. Intensive multidisciplinary treatment induced moderate weight loss and increased ghrelin secretion, but serum PYY and GLP-1 concentrations and insulin sensitivity remained unchanged.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • The addition of monosodium glutamate and inosine monophosphate-5 to high-protein meals: effects on satiety, and energy and macronutrient intakes. 19267954

    In a fed and orally stimulated state, whether the addition of monosodium glutamate (MSG) (alone or in combination with inosine monophosphate-5 (IMP-5)) to a high-protein (HP) meal leads to early satiety and a difference in energy intake at a second course was investigated. Ten men and twelve women consumed, in random order, a first-course meal consisting of: (1) water (control); (2) a HP meal with 0.6% MSG and 0.25% IMP-5; (3) a HP meal with no additives; (4) a HP meal with MSG only; (5) a sham-fed meal 2 (oral-stimulation). Appetite perceptions, plasma concentrations of glucagon-like peptide 1 (GLP-1), glucose and insulin, and energy intake at a buffet (i.e. a second course) were measured before and after each condition. Changes in appetite, and in GLP-1, glucose and insulin, were similar for the three fed HP conditions and all were greater (post hoc all P < 0.01) than the control and sham conditions. Energy intake was not different following the HP+MSG+IMP (1.86 (SEM 0.3) MJ) as compared with the HP+MSG-only (2.24 (SEM 0.28) MJ) condition (P = 0.08), or for the HP+MSG+IMP compared with the HP no-additives condition (1.60 (SEM 0.29) MJ) (P = 0.21). Following the HP+MSG-only condition, 0.64 (SEM 0.20) MJ more energy was consumed compared with the HP no-additives condition (P = 0.005). We conclude that the addition of MSG to a HP meal does not influence perceptions of satiety and it may increase energy intake at a second course. Cephalic responses after the sham condition were of similar magnitude to the control and therefore just tasting food is not enough to influence appetite and energy intake.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Decreased glucagon-like peptide 1 release after weight loss in overweight/obese subjects. 15897480

    OBJECTIVE: Postprandial glucagon-like peptide 1 (GLP-1) release seems to be attenuated in obese subjects. Results on whether weight loss improves GLP-1 release are contradictory. The aim of this study was to further investigate the effect of weight loss on basal and postprandial GLP-1 release in overweight/obese subjects. RESEARCH METHODS AND PROCEDURES: Thirty-two overweight/obese subjects participated in a repeated measurement design before (BMI, 30.3 +/- 2.8 kg/m2; waist circumference, 92.6 +/- 7.8 cm; hip circumference, 111.1 +/- 7.4 cm) and after a weight loss period of 6 weeks (BMI, 28.2 +/- 2.7 kg/m2; waist circumference, 85.5 +/- 8.5 cm; hip circumference, 102.1 +/- 9.2 cm). During weight loss, subjects received a very-low-calorie diet (Optifast) to replace three meals per day. Subjects came to the laboratory fasted, and after a baseline blood sample, received a standard breakfast (1.9 MJ). Postprandially, blood samples were taken every one-half hour relative to intake for 120 minutes to determine GLP-1, insulin, glucose, and free fatty acids from plasma. Appetite ratings were obtained with visual analog scales. RESULTS: After weight loss, postprandial GLP-1 concentrations at 30 and 60 minutes were significantly lower than before weight loss (p 0.05). Glucose concentrations were also lower, and free fatty acids were higher compared with before weight loss. Ratings of satiety were increased, and hunger scores were decreased after weight loss (p 0.05). DISCUSSION: In overweight/obese subjects, GLP-1 concentrations after weight loss were decreased compared with before weight loss, and nutrient-related stimulation was abolished. This might be a response to a proceeding negative energy balance. Satiety and GLP-1 seem to be unrelated in the long term.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Rectal taurocholate increases L cell and insulin secretion, and decreases blood glucose and food intake in obese type 2 diabetic volunteers. 22696033

    Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are secreted from enteroendocrine L cells in response to numerous stimuli, including bile salts. Both have multiple effects that are potentially useful in treating diabetes and obesity. L cell number and hormone content in the intestine are highest in the rectum in humans. We investigated the effects of intrarectal sodium taurocholate on plasma GLP-1, PYY, insulin and glucose concentrations, and on food intake of a subsequent meal.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Effects of oral fat perception by modified sham feeding on energy expenditure, hormones and appetite profile in the postprandial state. 18814804

    Previously, we have shown that satiety and metabolites increased after high-fat modified sham feeding (MSF). We assessed possible metabolic effects due to oral stimulation with a high-fat sham-fed 'meal', in comparison with a high-fat fed meal and with water, in the postprandial state. Fourteen healthy women (aged 18-40 years; BMI 22.5 (SD 3) kg/m2) were fed in energy balance during 4 d with a 50 % energy as carbohydrate, 15 % energy as protein and 35 % energy as fat menu. On day 4, subjects were given one out of three test lunches, 5 h after a high-fat breakfast, in random order: a high-fat MSF lunch, water (W) or the same lunch to be eaten (E), during their 36 h stay in the respiration chamber, where substrate oxidation, 24 h energy expenditure (EE) and appetite profile were measured. Oral fat stimulation by MSF increased EE (W 6.3 (SD 0.8) v. MSF 6.9 (SD 1.0) kJ/min and E 6.8 (SD 0.7) kJ/min; P < 0.04) for 1 h, increased plasma insulin concentrations (t = 15; W 10.0 (SD 3.4) v. MSF 13.2 (SD 4.0) v. E 22.3 (SD 3.3) units/l; P < 0.0001), attenuated changes in plasma NEFA concentrations (t = 15, W 432 (SD 108) v. MSF 418 (SD 146) v. E 282 (SD 72) micromol/l; P < 0.0001), plasma TAG concentrations (t = 60; W 1092 (SD 548) v. MSF 1116 (SD 493) micromol/l and E 1350 (SD 352) micromol/l; P < 0.02) and plasma glycerol concentrations (t = 15, W 87 (SD 29) v. MSF 74 (SD 34) micromol/l and E 67 (SD 18) micromol/l; P < 0.03). Over a longer period of time, MSF had no effects on substrate oxidation, diet-induced thermogenesis or total EE. In addition to the previously observed metabolic effects of oral stimulation with fat, EE is stimulated up to 1 h after the MSF meal.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA

  • Comparison of the effects of a high- and normal-casein breakfast on satiety, 'satiety' hormones, plasma amino acids and subsequent energy intake. 18634717

    The present study compared the effects of a high- and normal-casein-protein breakfast on satiety, 'satiety' hormones, plasma amino acid responses and subsequent energy intake. Twenty-five healthy subjects (BMI 23.9 (SEM 0.3) kg/m2; age 22 (SEM 1) years) received a subject-specific standardised breakfast (20% of daily energy requirements): a custard with casein as the single protein source with either 10, 55 and 35 (normal-casein breakfast) or 25, 55 and 20 (high-casein breakfast) % of energy (En%) from protein, carbohydrate and fat respectively in a randomised, single-blind design. Appetite profile (visual analogue scale; VAS), plasma glucose, insulin, glucagon-like peptide 1, ghrelin and amino acid concentrations were determined for 4 h; here the sensitive moment in time for lunch was determined. Subjects came for a second set of experiments and received the same custards for breakfast, and an ad libitum lunch was offered at 180 min after breakfast; energy intake was assessed. There were increased scores of fullness and satiety after the 25 En% casein-custard compared with the 10 En% casein-custard, particularly at 180 min (26 (SEM 4) v. 11 (SEM 5) mm VAS; P0.01) and 240 min (13 (SEM 5) v. -1 (SEM 5) mm VAS; P0.01). This coincided with prolonged elevated plasma amino acid concentrations; total amino acids and branched-chain amino acids were higher after the 25 En% casein-custard compared with the 10 En% casein-custard at 180 and 240 min (P0.001). There was no difference in energy intake (3080 (SEM 229) v. 3133 (SEM 226) kJ for 25 En% and 10 En% respectively; NS) from the ad libitum lunch. In conclusion, a breakfast with 25% of energy from casein is rated as being more satiating than a breakfast with 10% of energy from casein at 3 and 4 h after breakfast, coinciding with prolonged elevated concentrations of plasma amino acids, but does not reduce subsequent energy intake.
    Document Type:
    Reference
    Product Catalog Number:
    EGLP-35K
    Product Catalog Name:
    Glucagon Like Peptide-1 (Active) ELISA