Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats

Donahey, Jamie C. K.; Dijk, Gertjan van; Woods, Stephen C.; Seeley, Randy J.

doi:10.1016/s0006-8993(97)01057-3

Cited by 107 publications

(78 citation statements)

References 18 publications

(4 reference statements)

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“…Continuous administration of other anorexigenic peptides (cholecystokinin, amylin, GLP-1) by osmotic minipump has also been reported to produce either no effect or a transient reduction in daily food intake in rodents (2,4,11,12,25). One possible explanation for these transient responses is that early peptide-induced reductions in daily food intake and adiposity elicit a delayed compensatory response to restore energy balance mediated by a reduction in leptin signaling to the brain (2,17).…”

Section: Discussionmentioning

confidence: 99%

Daily, intermittent intravenous infusion of peptide YY(3-36) reduces daily food intake and adiposity in rats

Chelikani

Haver²,

Reeve³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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reduces food intake and weight gain in rats when injected into the peritoneal cavity twice daily for 7 days. Numerous laboratories have failed to confirm that daily injections of PYY(3-36) decrease body weight. Continuous subcutaneous administration of PYY(3-36) by osmotic minipump has been reported to reduce daily food intake in rodents but only during the first 3-4 days of administration. Here we show the effects of different daily patterns of intravenous infusion of PYY(3-36) on food intake, body weight, and adiposity in rats tethered via infusion swivels to computercontrolled pumps. Measurement of food bowl weight recorded by computer every 20 s permitted daily assessment of the instantaneous effects of PYY(3-36) administration on food intake and meal patterns. One-hour intravenous infusions of PYY(3-36) at 30 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 every other hour for 10 days produced a sustained reduction in daily food intake of ϳ20% and decreased body weight and adiposity by 7 and 35%, respectively. Thus dosage pattern is critical for producing a sustained effect of PYY(3-36) on food intake and adiposity.gastrointestinal; body weight; body composition THE GASTROINTESTINAL SYSTEM plays an important sensing and signaling role in control of food intake and regulation of energy reserves (5). A growing number of peptide signals of gastric, intestinal, and pancreatic origin have been shown to inhibit short-term food intake when administered acutely to experimental animals and humans. These include cholecystokinin, amylin, glucagon-like peptide-1 (GLP-1), oxyntomodulin, peptide YY(3-36) ], pancreatic polypeptide, gastrinreleasing peptides (GRPs) GRP-27 and GRP-

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Section: Discussionmentioning

confidence: 99%

Daily, intermittent intravenous infusion of peptide YY(3-36) reduces daily food intake and adiposity in rats

Chelikani

Haver²,

Reeve³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Consistent with this idea are our findings that, relative to controls, i3vt GLP-1 treatment over several days, either by osmotic minipump (delivering 30 µg GLP-1/day), or i3vt injections (15 µg twice per day, each prior to a 2-h window in which animals were allowed to feed) reduced food intake only during the first treatment day, but never affected body weight. 40 Thus, like CCK, i3vt administration of GLP-1 potently reduces the size of the subsequent meal, but the total daily food intake is not different from that of controls. Thus, if GLP-1 in the CNS does have a role as a control of food intake, it would appear to be as a shortterm satiety signal and not a long-term regulator of caloric intake and body weight.…”

Section: Glp-1 Reduces Short-term Food Intakementioning

confidence: 97%

“…GLP-1 receptor deficient mice have normal body weights, 10 while it is well known that leptin receptor-deficient rodents (db/db mice, fa/fa Zucker rats) become morbidly obese. Since animals with a deficiency in leptin signaling respond normally to both i3vt GLP or CCK to reduce short-term food intake, however, without changing daily caloric intake or body weight, 40,47 aberrant CCK or GLP-1 receptor functioning does not underlie the obese phenotype in leptin-receptor deficient rodents.…”

Section: Glp-1 Reduces Short-term Food Intakementioning

confidence: 99%

Glucagon-like peptide-1 (7–36) amide: a central regulator of satiety and interoceptive stress

Dijk

Thiele

1999

Neuropeptides

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INTRODUCTIONIngestion of food is a necessary and pleasant occupation that allows humans and other species to maintain caloric homeostasis and a certain level of body weight. Ironically, in doing so, one's 'milieu interieur' is put at risk because meal-induced fuel excursions can have deleterious effects on metabolic (e.g. glycosylation causing loss of enzymatic efficacy) and cardiovascular (e.g. triglyceride accumulation, increased blood pressure, etc.) processes. 1,2 To reduce these perturbations to a minimum, evolution has provided many species (including humans and rodents) with a fine-tuned system enabling ingested nutrients to be anticipated, efficiently digested, and stored. 3 One of these mechanisms includes passage of nutrients through the digestive tract, triggering the release of a number of peptides from endocrine cells located in the wall of various parts of the gastrointestinal tract. These peptides serve important functions in facilitating the process of nutrient digestion/storage. Among these, the truncated (i.e. 7-36) amidated form of glucagon-like peptide-1 (GLP-1) has attracted considerable attention over the last several years. Firstly, because of its remarkable peripheral insulinotropic effects that could be useful for clinical purposes. Secondly, because more recent data suggest an important role of this peptide in the central nervous system (CNS) control of ingestive behavior. Although the present paper mainly focusses on the latter issue, a short review of peripheral GLP mechanisms is necessary for a better understanding of the processes that relate GLP-1 to food intake. GLP-1 FROM THE GASTROINTESTINAL TRACTGLP-1 is processed from proglucagon in mucosal L cells of the distal portion of the ileum and in the A cells of the pancreas. Ingested food, particularly when rich in carbohydrates, causes the level of circulating GLP-1 (mainly of ileal origin) to increase, and in turn, GLP-1 potently stimulates the secretion of insulin from pancreatic B cells via receptor-mediated processes (for reviews, see refs 4 and 5). In contrast, it reduces the secretion of glucagon, at least under ad libitum feeding conditions. 6 While GLP-1 may have some direct stimulatory effects on glucose clearance in peripheral tissue 7,8 (presumably via activation of specific GLP-1 receptors in liver, muscle, kidney Summary Glucagon-like peptide-1 (7-36) amide (GLP-1) is processed from proglucagon in the distal ileum as well as in the CNS. In the periphery, GLP-1 acts as an incretin factor and profoundly inhibits upper gastrointestinal motility ('ileal brake'), the latter presumably involving the CNS. Within the CNS, GLP-1 has a satiating effect, since administration of GLP-1 into the third cerebral ventricle reduces short-term food intake (and meal size), while administration of GLP-1 antagonists have the opposite effect. In addition, activation of GLP-1 receptors in certain brain regions elicits strong taste aversions. Similarities between toxin-and GLP-1-induced neuronal activity in the CNS (brain stem) suggest a role f...

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“…In addition to the deceleration of gastric emptying, GLP-1 is involved in regulating satiety, as shown in normal-weight and obese men infused with GLP-1 (17,33,34). GLP-1 also decreases food intake; by contrast, central administration of the GLP-1 receptor (GLP-1R) antagonist exendin-(9-39) stimulates food intake (14,54).…”

mentioning

confidence: 99%

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

Kumar¹,

Byerley²,

Vólaufová³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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We demonstrated previously that food intake traits map to a quantitative trait locus (QTL) on proximal chromosome 17, which encompasses Glp1r (glucagon-like peptide 1 receptor), encoding an important modulator of gastric emptying. We then confirmed this QTL in a B6.CAST-17 congenic strain that consumed 27% more carbohydrate and 17% more total calories, yet similar fat calories, per body weight compared with the recipient C57BL/6J. The congenic strain also consumed greater food volume. The current aims were to 1) identify genetic linkage for total food volume in F 2 mice, 2) perform gene expression profiling in stomach of B6.CAST-17 congenic mice using oligonucleotide arrays, 3) test for allelic imbalance in Glp1r expression, 4) evaluate gastric emptying rate in parental and congenic mice, and 5) investigate a possible effect of genetic variation in Glp1r on gastric emptying. A genome scan revealed a single QTL for total food volume (Tfv1) (log of the odds ratio ϭ 7.6), which was confirmed in B6.CAST-17 congenic mice. Glp1r exhibited allelic imbalance in stomach, which correlated with accelerated gastric emptying in parental CAST and congenic B6.CAST-17 mice. Moreover, congenic mice displayed an impaired gastric emptying response to exendin-(9-39). These results suggest that genetic variation in Glp1r contributes to the strain differences in gastric emptying rate.quantitative trait locus; glucagon-like peptide 1 receptor THE GUT HORMONE GLUCAGON-LIKE PEPTIDE 1 (GLP-1) inhibits gastric emptying, reduces postprandial gastric secretion, and may play a physiological role in regulating appetite and energy intake. Systemic administration of GLP-1 in physiological amounts in both humans and animals potently inhibits gastric emptying (9,13,15,31,59,61), and this effect can be blocked by administration of the GLP-1 receptor antagonist exendin (9-39) (21). The mechanism by which GLP-1 inhibits gastric emptying is thought to involve receptors located either in the central nervous system or associated with afferent pathways to the brain stem (9,21,60). In addition to the deceleration of gastric emptying, GLP-1 is involved in regulating satiety, as shown in normal-weight and obese men infused with 33,34). GLP-1 also decreases food intake; by contrast, central administration of the GLP-1 receptor (GLP-1R) antagonist exendin-(9-39) stimulates food intake (14, 54).The GLP-1R is a seven-transmembrane domain receptor belonging to the B family of G-protein-coupled receptors (6, 52). The GLP-1R recognizes GLP-1 specifically and does not show demonstrable binding by related peptides (Ref. 52; for review, see Ref. 6). In rodents, GLP-1 receptor mRNA and high-affinity GLP-1 binding sites have been identified in pancreatic islets, in gastrointestinal tract, in lung, in kidney, in heart, and throughout the brain (7,8,16). The satiety-promoting effects of GLP-1 implicate Glp1r as a physiological gene candidate for ingestive behavior phenotypes (1).Glp1r maps to the peak of a genetic region containing overlapping quantitative trait loci (Q...

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Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats

Cited by 107 publications

References 18 publications

Daily, intermittent intravenous infusion of peptide YY(3-36) reduces daily food intake and adiposity in rats

Daily, intermittent intravenous infusion of peptide YY(3-36) reduces daily food intake and adiposity in rats

Glucagon-like peptide-1 (7–36) amide: a central regulator of satiety and interoceptive stress

Genetic variation inGlp1rexpression influences the rate of gastric emptying in mice

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