The Effect of Soluble Fiber Dextrin on Subjective and Physiological Markers of Appetite: A Randomized Trial

Obesity is a leading public health problem throughout the world. The development of foods that increase satiety and reduce food may aid weight management. This study determined the effect of consuming soluble fiber dextrin (SFD) on appetite, appetitive hormones, breath hydrogen and food intake in adults. Forty-three participants completed this study. For each treatment, 50% of the SFD was provided in liquid form as part of breakfast and 50% in solid form as a morning snack. Appetite questionnaires, blood and breath samples were collected immediately before breakfast and at regular intervals during the test session. The participants consumed an ad libitum lunch meal, afternoon snack and dinner meal, and the amount eaten was recorded. Following dinner, participants left the laboratory but were required to keep a diet diary for the remainder of the day. Breath hydrogen concentration was significantly higher following the consumption of SFD compared to control (p < 0.05). There was no observed overall treatment effect of consuming SFD on GLP-1 (Glucagon-Like-Peptide-1), ghrelin, CCK-8 (Cholecystokinin) or PYY3-36 (Petptide YY) (p > 0.05). Moreover, consuming foods containing SFD had no effect on subjective appetite or food intake (p > 0.05). Consuming foods containing SFD increased breath hydrogen but did not influence food intake, appetite or appetitive hormones. However, the limitations of this study may have individually or collectively masked an effect of SFD on food intake and appetite.

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Central glucagon-like peptide 1 receptor-induced anorexia requires glucose metabolism-mediated suppression of AMPK and is impaired by central fructose

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00446.2012 ◽

2013 ◽

Vol 304 (7) ◽

pp. E677-E685 ◽

Cited By ~ 34

Author(s):

Melissa A. Burmeister ◽

Jennifer Ayala ◽

Daniel J. Drucker ◽

Julio E. Ayala

Keyword(s):

Food Intake ◽

Glucose Metabolism ◽

Dependent Manner ◽

Anorectic Effect ◽

Dependent Inhibition ◽

Glycolytic Inhibitor ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Amp Activated Protein Kinase ◽

Mediated Reduction

Glucagon-like peptide-1 (GLP-1) suppresses food intake via activation of a central (i.e., brain) GLP-1 receptor (GLP-1R). Central AMP-activated protein kinase (AMPK) is a nutrient-sensitive regulator of food intake that is inhibited by anorectic signals. The anorectic effect elicited by hindbrain GLP-1R activation is attenuated by the AMPK stimulator AICAR. This suggests that central GLP-1R activation suppresses food intake via inhibition of central AMPK. The present studies examined the mechanism(s) by which central GLP-1R activation inhibits AMPK. Supporting previous findings, AICAR attenuated the anorectic effect elicited by intracerebroventricular (icv) administration of the GLP-1R agonist exendin-4 (Ex-4). We demonstrate that Ex-4 stimulates glycolysis and suppresses AMPK phosphorylation in a glucose-dependent manner in hypothalamic GT1-7 cells. This suggests that inhibition of AMPK and food intake by Ex-4 requires central glucose metabolism. Supporting this, the glycolytic inhibitor 2-deoxyglucose (2-DG) attenuated the anorectic effect of Ex-4. However, icv glucose did not enhance the suppression of food intake by Ex-4. AICAR had no effect on Ex-4-mediated reduction in locomotor activity. We also tested whether other carbohydrates affect the anorectic response to Ex-4. Intracerebroventricular pretreatment with the sucrose metabolite fructose, an AMPK activator, attenuated the anorectic effect of Ex-4. This potentially explains the increased food intake observed in sucrose-fed mice. In summary, we propose a model whereby activation of the central GLP-1R reduces food intake via glucose metabolism-dependent inhibition of central AMPK. We also suggest that fructose stimulates food intake by impairing central GLP-1R action. This has significant implications given the correlation between sugar consumption and obesity.

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Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00243.2015 ◽

2016 ◽

Vol 310 (10) ◽

pp. R906-R916 ◽

Cited By ~ 9

Author(s):

Alison D. Kreisler ◽

Linda Rinaman

Keyword(s):

Food Intake ◽

Potential Role ◽

Liquid Diet ◽

Neural Activation ◽

Intracerebroventricular Injection ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Diet Intake ◽

Published Research ◽

Diet Type

Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ∼11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ∼14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.

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GPR40 reduces food intake and body weight through GLP-1

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00435.2016 ◽

2017 ◽

Vol 313 (1) ◽

pp. E37-E47 ◽

Cited By ~ 16

Author(s):

Judith N. Gorski ◽

Michele J. Pachanski ◽

Joel Mane ◽

Christopher W. Plummer ◽

Sarah Souza ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Food Intake ◽

Partial Agonist ◽

Glucose Lowering ◽

Partial Agonists ◽

Lower Glucose ◽

Glucagon Like Peptide 1 ◽

Glucose Stimulated Insulin Secretion ◽

G Protein Coupled

G protein-coupled receptor 40 (GPR40) partial agonists lower glucose through the potentiation of glucose-stimulated insulin secretion, which is believed to provide significant glucose lowering without the weight gain or hypoglycemic risk associated with exogenous insulin or glucose-independent insulin secretagogues. The class of small-molecule GPR40 modulators, known as AgoPAMs (agonist also capable of acting as positive allosteric modulators), differentiate from partial agonists, binding to a distinct site and functioning as full agonists to stimulate the secretion of both insulin and glucagon-like peptide-1 (GLP-1). Here we show that GPR40 AgoPAMs significantly increase active GLP-1 levels and reduce acute and chronic food intake and body weight in diet-induced obese (DIO) mice. These effects of AgoPAM treatment on food intake are novel and required both GPR40 and GLP-1 receptor signaling pathways, as demonstrated in GPR40 and GLP-1 receptor-null mice. Furthermore, weight loss associated with GPR40 AgoPAMs was accompanied by a significant reduction in gastric motility in these DIO mice. Chronic treatment with a GPR40 AgoPAM, in combination with a dipeptidyl peptidase IV inhibitor, synergistically decreased food intake and body weight in the mouse. The effect of GPR40 AgoPAMs on GLP-1 secretion was recapitulated in lean, healthy rhesus macaque demonstrating that the putative mechanism mediating weight loss translates to higher species. Together, our data indicate effects of AgoPAMs that go beyond glucose lowering previously observed with GPR40 partial agonist treatment with additional potential for weight loss.

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Soluble Fiber with High Water-Binding Capacity, Swelling Capacity, and Fermentability Reduces Food Intake by Promoting Satiety Rather Than Satiation in Rats

Nutrients ◽

10.3390/nu8100615 ◽

2016 ◽

Vol 8 (10) ◽

pp. 615 ◽

Cited By ~ 7

Author(s):

Chengquan Tan ◽

Hongkui Wei ◽

Xichen Zhao ◽

Chuanhui Xu ◽

Yuanfei Zhou ◽

...

Keyword(s):

Food Intake ◽

Binding Capacity ◽

High Water ◽

Soluble Fiber ◽

Water Binding ◽

Swelling Capacity

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UNDERWEIGHT, STUNTING, WASTING DAN KAITANNYA TERHADAP ASUPAN MAKAN, PENGETAHUAN IBU, DAN PEMANFAATAN PELAYANAN KESEHATAN

JURNAL RISET GIZI ◽

10.31983/jrg.v8i2.6329 ◽

2020 ◽

Vol 8 (2) ◽

pp. 101-106

Author(s):

Risky Amelia Rhamadani ◽

Reny Noviasty ◽

Ratno Adrianto

Keyword(s):

Public Health ◽

Food Intake ◽

Health Services ◽

Nutritional Status ◽

Positive Relationship ◽

Complementary Feeding ◽

Health Centre ◽

Public Health Problem ◽

Significant Positive Relationship ◽

Utilization Of Health Services

Background : Nutrition problems in toddlers become a public health problem when it exceeds WHO indicators in which the issue of malnutrition and undernutrition 17.8%, short toddlers 27.5% and thin toddlers 11.1%. The problem of undernutrition, short and thin toddlers are public health problem in the chronic category.Objective : to determine the factor related to the nutritional status of toddlers in Loa Ipuh Health Centre. The design of this research is a cross-sectional study with total sample of 97 toddlers. Data collection uses anthropometric measurements, 24 hours of form food recall and questionnaires for mother's knowledge of breastfeeding complementary feeding and the utilization of health services.Method : Data analysis is using Pearson product-moment test with a significance level of 0.05. The results showed that there was a significant positive relationship between the food intake with the WAZ (P=0,000), HAZ (P=0,000) and WHZ (P=0,021), mother's knowledge about complementary feeding with the WAZ (P=0,041), HAZ (P=0,010) and WHZ (P=0,010), utilization of health services with the WAZ (P=0,007), HAZ (P=0,009) and WHZ (P=0,006). Result : there is a significant positive relationship between intake of toddler feeding, mother's knowledge about complementary feeding and the utilization of health services with the nutritional status of toddlers WAZ, HAZ, and WHZ. Access to health services should be improved and evenly distributed throughout the health centre area.Conclusion : There is a significant positive relationship between food intake for children under five, maternal knowledge about complementary foods and health service utilization with the nutritional status

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A Non-targeted Approach to Chemical Discrimination Between Green Tea Dietary Supplements and Green Tea Leaves by HPLC/MS

Journal of AOAC International ◽

10.1093/jaoac/94.2.487 ◽

2011 ◽

Vol 94 (2) ◽

pp. 487-497 ◽

Cited By ~ 6

Author(s):

Jianghao Sun ◽

Pei Chen ◽

Long-Ze Lin ◽

James M Harnly

Keyword(s):

Dietary Supplements ◽

Green Tea ◽

Similarity Coefficients ◽

Tea Leaves ◽

Liquid Form ◽

Epicatechin Gallate ◽

Accurate Mass Measurements ◽

Chemical Discrimination ◽

Green Tea Leaves ◽

Solid Form

Abstract Green tea-based dietary supplements (GTDSs) have gained popularity in the U.S. market in recent years. This study evaluated the phytochemical composition difference of GTDS in comparison with green tea leaves using an HPLC/MS fingerprinting technique coupled with chemometric analysis. Five components that are most responsible for class separation among samples were identified as (-) epicatechin gallate, strictinin, trigalloylglucose, quercetin-3-O-glucosylrhamnosylglucoside, and kaempferol-3-O-galactosyl-rhamnosylglucoside, according to the accurate mass measurements and MS/MS data. The similarity coefficients between the GTDSs in solid form with green tea were 0.55 to 0.91, while for the GTDSs in liquid form they were 0.12 to 0.89, which suggested that chemical composition variance across the GTDSs was significant. Flavonol aglycone concentrations were higher in GTDSs than in tea leaves, indicating the degradation of flavonol glycosides or the oxidation of catechin during the manufacturing and storage processes. In some GTDS samples, compounds were identified that were on the label. The results demonstrate the urgency of QC for GTDS products.

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Deletion of GPR40 fatty acid receptor gene in mice blocks mercaptoacetate-induced feeding

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00548.2015 ◽

2016 ◽

Vol 310 (10) ◽

pp. R968-R974 ◽

Cited By ~ 2

Author(s):

Ai-Jun Li ◽

Michael F. Wiater ◽

Qing Wang ◽

Stephen Wank ◽

Sue Ritter

Keyword(s):

Fatty Acid ◽

Food Intake ◽

Receptor Gene ◽

Treatment Groups ◽

Metabolic Monitoring ◽

Afferent Activation ◽

Inhibit Food Intake ◽

Vagal Afferent ◽

Glucagon Like Peptide 1 ◽

G Protein Coupled

Both increased and decreased fatty acid (FA) availability contribute to control of food intake. For example, it is well documented that intestinal FA reduces feeding by triggering enterondocrine secretion of satietogenic peptides, such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1). In contrast, mechanisms by which decreased FA availability increase feeding are not well understood. Over the past three decades substantial research related to FA availability and increased feeding has involved use of the orexigenic compound mercaptoacetate (MA). Because MA reportedly inhibits FA oxidation, it has been assumed that reduced FA oxidation accounts for the orexigenic action of MA. Recently, however, we demonstrated that MA antagonizes G protein-coupled receptor 40 (GPR40), a membrane receptor for long and medium chain FA. We also demonstrated that, by antagonizing GPR40, MA inhibits GLP-1 secretion and attenuates vagal afferent activation by FA. Because both vagal afferent activation and GLP-1 inhibit food intake, we postulated that inhibition of GPR40 by MA might underlie the orexigenic action of MA. We tested this hypothesis using male and female GPR40 knockout (KO) and wild-type (WT) mice. Using several testing protocols, we found that MA increased feeding in WT, but not GPR40 KO mice, and that GPR40 KO mice gained more weight than WT on a high-fat diet. Metabolic monitoring after MA or saline injection in the absence of food did not reveal significant differences in respiratory quotient or energy expenditure between treatment groups or genotypes. These results support the hypothesis that MA stimulates food intake by blocking FA effects on GPR40.

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The common hepatic branch of the vagus is not required to mediate the glycemic and food intake suppressive effects of glucagon-like-peptide-1

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00356.2011 ◽

2011 ◽

Vol 301 (5) ◽

pp. R1479-R1485 ◽

Cited By ~ 55

Author(s):

Matthew R. Hayes ◽

Scott E. Kanoski ◽

Bart C. De Jonghe ◽

Theresa M. Leichner ◽

Amber L. Alhadeff ◽

...

Keyword(s):

Food Intake ◽

Vagal Afferents ◽

Oral Glucose ◽

Afferent Fibers ◽

The Common ◽

Vagal Afferent ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

And Control ◽

Hepatic Branch

The incretin and food intake suppressive effects of intraperitoneally administered glucagon-like peptide-1 (GLP-1) involve activation of GLP-1 receptors (GLP-1R) expressed on vagal afferent fiber terminals. Central nervous system processing of GLP-1R-driven vagal afferents results in satiation signaling and enhanced insulin secretion from pancreatic-projecting vagal efferents. As the vast majority of endogenous GLP-1 is released from intestinal l-cells following ingestion, it stands to reason that paracrine GLP-1 signaling, activating adjacent GLP-1R expressed on vagal afferent fibers of gastrointestinal origin, contributes to glycemic and food intake control. However, systemic GLP-1R-mediated control of glycemia is currently attributed to endocrine action involving GLP-1R expressed in the hepatoportal bed on terminals of the common hepatic branch of the vagus (CHB). Here, we examine the hypothesis that activation of GLP-1R expressed on the CHB is not required for GLP-1's glycemic and intake suppressive effects, but rather paracrine signaling on non-CHB vagal afferents is required to mediate GLP-1's effects. Selective CHB ablation (CHBX), complete subdiaphragmatic vagal deafferentation (SDA), and surgical control rats received an oral glucose tolerance test (2.0 g glucose/kg) 10 min after an intraperitoneal injection of the GLP-1R antagonist, exendin-(9–39) (Ex-9; 0.5 mg/kg) or vehicle. CHBX and control rats showed comparable increases in blood glucose following blockade of GLP-1R by Ex-9, whereas SDA rats failed to show a GLP-1R-mediated incretin response. Furthermore, GLP-1(7–36) (0.5 mg/kg ip) produced a comparable suppression of 1-h 25% glucose intake in both CHBX and control rats, whereas intake suppression in SDA rats was blunted. These findings support the hypothesis that systemic GLP-1R mediation of glycemic control and food intake suppression involves paracrine-like signaling on GLP-1R expressed on vagal afferent fibers of gastrointestinal origin but does not require the CHB.

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