Energy expenditure by intravenous administration of glucagon-like peptide-1 mediated by the lower brainstem and sympathoadrenal system

Osaka, Toshimasa; Endo, M; Yamakawa, Midori; Inoue, Shuji

doi:10.1016/j.peptides.2005.02.016

Cited by 69 publications

(49 citation statements)

References 28 publications

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“…Several studies in rodents and humans have provided contradictory evidence as to whether glucagon-like peptide-1 has a stimulatory or inhibitory effect on energy expenditure. [28][29][30][31] To date this is the first study investigating the effect of a gut peptide on 'free-living' energy expenditure in human volunteers.…”

Section: Discussionmentioning

confidence: 99%

Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial

et al. 2006

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Background: Oxyntomodulin has recently been found to decrease body-weight in obese humans and may be a potential antiobesity therapy. Objective: To determine whether oxyntomodulin alters energy expenditure, in addition to reducing energy intake, in 'freeliving' overweight and obese volunteers. Design: Randomized double-blind controlled cross-over trial. Setting: Community and hospital-based. Participants: Fifteen healthy overweight and obese men and women (age: 23-49 years, BMI: 25.1-39.0 kg/m 2 ). All volunteers completed the study protocol. Interventions: Four-day subcutaneous self-administration of pre-prandial oxyntomodulin, three times daily. Participants were advised to maintain their normal dietary and exercise regimen. Measurements: (1) Energy expenditure, measured by indirect calorimetry and combined heart rate and movement monitoring; (2) energy intake, measured during a study meal. Results: Oxyntomodulin administration reduced energy intake at the study meal by 128729 kcal (P ¼ 0.0006) or 17.375.5% (P ¼ 0.0071), with no change in meal palatability. Oxyntomodulin did not alter resting energy expenditure; but increased activity-related energy expenditure by 1437109 kcal/day or 26.279.9% (P ¼ 0.0221); total energy expenditure by 9.474.8% (P ¼ 0.0454) and physical activity level by 9.574.6% (P ¼ 0.0495). A reduction in body weight of 0.570.2% was observed during the oxyntomodulin administration period (P ¼ 0.0232). Conclusion: Oxyntomodulin increases energy expenditure while reducing energy intake resulting in negative energy balance. This data supports the role of oxyntomodulin as a potential anti-obesity therapy.

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Section: Discussionmentioning

confidence: 99%

Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial

et al. 2006

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“…Somatostatin inhibits GIP and GLP-1 secretion from small intestinal cultures through SSTR5 [17]. Peripheral GLP-1 receptor ligand administration caused tachycardia [20,21], but exendin-(9-39), the GLP-1 receptor antagonist, blocked the response in rats [22]. Yamamoto et al reported the relation between GLP-1 and early dumping syndrome.…”

Section: Fig 2 Continuous Glucose Monitoring (Cgm) Over 24 Hoursmentioning

confidence: 99%

Octreotide improves early dumping syndrome potentially through incretins: a case report

et al. 2013

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Dumping synDrome, or rapid gastric emptying, is a serious complication that may occur after gastric surgery in approximately 5-10% of patients, although it may occur in approximately 20% after vagotomy with pyloroplasty and up to 50% after esophagectomy [1][2][3]. In spite of this level of occurrence, the pathophysiologic mechanisms underlying the symptoms of dumping syndrome are poorly understood. Here, we report a patient with dumping syndrome following distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. In this case, we have measured the levels of several hormones during a 75g oral glucose tolerance test (75g-OGTT), and found that glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were both inhibited by octreotide treatment. Abstract. Dumping syndrome, or rapid gastric emptying, is a frequent complication after gastric surgery. In this case, the patient was a 47-year-old woman who 10 years previously had undergone distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. She presented with symptoms of weakness, headache, palpitation, sweating, dizziness and significant fatigue between one and two hours after a meal. Because a 75g oral glucose tolerance test (75g-OGTT) induced both acute postprandial tachycardia (within 1 hour) and postprandial hypoglycemia, we diagnosed this patient with early and late dumping syndrome. Dietary measures and acarbose improved symptoms of late dumping syndrome but did not prevent the symptoms of early dumping syndrome such as postprandial tachycardia, weakness, headache, palpitation, and dizziness. We therefore used the somatostatin analogue octreotide, which has been reported as an effective therapy for early dumping syndrome. Octreotide prevented the symptoms of early dumping syndrome, especially postprandial tachycardia, but caused postprandial hyperglycemia. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75g-OGTT following subcutaneous injection of octreotide. No change was observed in vasoactive intestinal polypeptide (VIP), which is the gastrointestinal peptide hormone generally responsible for early dumping syndrome, suggesting possible contribution of incretins in early dumping syndrome of this patient.Key words: Dumping syndrome, GLP-1, Octreotide material and methods Laboratory analysesBlood samples were taken after an overnight fast. Plasma glucose concentrations were measured with the hexokinase G6PD UV method. Serum insulin concentrations were measured with a chemiluminescent enzyme immunoassay. Serum triglyceride concentrations were determined by Enzymatic method. Serum total cholesterol concentrations were measured by a cholesterol dehydrogenase ultraviolet method. Serum HDL cholesterol concentrations were determined by a direct method (Cholestest ® N HDL, Sekisui Medical, Japan). Hemoglobin A1c (NGSP) levels were measured by high performance liquid chromatographic assay (HPLC). Serum total GIP and...

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“…9,10 Endogenous release or intraperitoneal GLP-1R agonist delivery triggers a set of responses that include reduced food intake, [11][12][13][14] inhibition of gastric emptying, 9,14 stimulation of glucosedependent insulin secretion 15,16 and tachycardia. [17][18][19][20][21] GLP-1R ligand is also supplied by proglucagon-expressing neurons of the caudal brainstem that project to GLP-1Rs, which are distributed throughout the brain. [22][23][24] It is interesting to note that stimulation of central GLP-1R results in many of the same responses, for example, inhibition of food intake and increased insulin secretion, as are observed following peripheral ligand injection.…”

Section: Glp-1mentioning

confidence: 99%

“…The vagally transmitted effects of peripheral GLP-1R stimulation therefore involve behavioral and autonomic effector pathways that are downstream of CNS processing. [17][18][19]21,25 Structures in the ascending visceral afferent pathway, which includes nuclei of the caudal brainstem (NTS; parabrachial nucleus), hypothalamus (lateral hypothalamus; paraventricular nucleus) and basal forebrain (bed nucleus of stria terminalis; central nucleus of the amygdala), 26,27 may therefore play a role in mediating responses triggered by peripheral GLP-1R agonist treatmentA role. Similarly for the central GLP-1 system, direct central GLP-1R ligand administration activates neurons in many of the same central structures that show GLP-1-binding 23 and/or express GLP-1R mRNA.…”

Section: Glp-1mentioning

confidence: 99%

The nucleus tractus solitarius: a portal for visceral afferent signal processing, energy status assessment and integration of their combined effects on food intake

2009

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For humans and animal models alike there is general agreement that the central nervous system processing of gastrointestinal (GI) signals arising from ingested food provides the principal determinant of the size of meals and their frequency. Despite this, relatively few studies are aimed at delineating the brain circuits, neurochemical pathways and intracellular signals that mediate GI-stimulation-induced intake inhibition. Two additional motivations to pursue these circuits and signals have recently arisen. First, the success of gastric-bypass surgery in obesity treatment is highlighting roles for GI signals such as glucagon-like peptide-1 (GLP-1) in intake and energy balance control. Second, accumulating data suggest that the intakereducing effects of leptin may be mediated through an amplification of the intake-inhibitory effects of GI signals. Experiments reviewed show that: (1) the intake-suppressive effects of a peripherally administered GLP-1 receptor agonist is mediated by caudal brainstem neurons and that forebrain-hypothalamic neural processing is not necessary for this effect; (2) a population of medial nucleus tractus solitarius (NTS) neurons that are responsive to gastric distention is also driven by leptin; (3) caudal brainstem-targeted leptin amplifies the food-intake-inhibitory effects of gastric distention and intestinal nutrient stimulation; (4) adenosine monophosphate-activated protein kinase (AMPK) activity in NTS-enriched brain lysates is elevated by food deprivation and reduced by refeeding and (5) the intake-suppressive effect of hindbrain-directed leptin is reversed by elevating hindbrain AMPK activity. Overall, data support the view that the NTS and circuits within the hindbrain mediate the intake inhibition of GI signals, and that the effects of leptin on food intake result from the amplification of GI signal processing.

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Energy expenditure by intravenous administration of glucagon-like peptide-1 mediated by the lower brainstem and sympathoadrenal system

Cited by 69 publications

References 28 publications

Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial

Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial

Octreotide improves early dumping syndrome potentially through incretins: a case report

The nucleus tractus solitarius: a portal for visceral afferent signal processing, energy status assessment and integration of their combined effects on food intake

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