scholarly journals Long-term CCK-leptin synergy suggests a role for CCK in the regulation of body weight

1999 ◽  
Vol 276 (4) ◽  
pp. R1038-R1045 ◽  
Author(s):  
Claire A. Matson ◽  
Robert C. Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Intraperitoneal Injection ◽  
Sucrose Intake ◽  
Reduced Body ◽  
Single Intraperitoneal Injection

The gut peptide CCK is a nutrient-related signal important to the control of food intake. In the present studies, we observed that a single intraperitoneal injection of CCK (1–2 μg/kg) given 2–3 h after intracerebroventricular leptin (2–5 μg) reduced body weight and chow intake over the ensuing 48 h more than did leptin alone. CCK alone had no effect on either 48-h chow intake or body weight but significantly reduced feeding during a 30-min sucrose test. However, reduction of 30-min sucrose intake by CCK was not enhanced by prior intracerebroventricular leptin. The present data suggest that CCK can contribute to the regulation of body weight when central leptin levels are elevated.

scholarly journals Effects of Acute Changes in Neonatal Leptin Levels on Food Intake and Long-Term Metabolic Profiles in Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (11) ◽  
pp. 4116-4126 ◽  
Author(s):  
Miriam Granado ◽  
Cristina García-Cáceres ◽  
Esther Fuente-Martín ◽  
Francisca Díaz ◽  
Virginia Mela ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Leptin Receptor ◽  
Uncoupling Protein ◽  
Metabolic Effects ◽  
Metabolic Profiles ◽  
Mrna Levels ◽  
Reduced Body ◽  
Acute Changes

In rodents there is a rise in serum leptin levels between postnatal days (PND) 5 and 14, with this neonatal leptin surge reported to modulate the maturation of hypothalamic circuits involved in appetite regulation. We hypothesized that acute changes in neonatal leptin levels have different long-term metabolic effects depending on how and when this surge is modified. To advance the timing of the normal leptin peak, male Wistar rats were injected with leptin (sc, 3 μg/g) on PND 2. To ablate the leptin peak on PND 10, a pegylated leptin antagonist (sc, 9 μg/g) was injected. Controls received vehicle. All rats were allowed to eat ad libitum until PND 150. Increased leptin on PND 2 reduced food intake (P < 0.01) after 3 months of age with no effect on body weight. Levels of total ghrelin were reduced (P < 0.001) and acylated ghrelin increased (P < 0.05), with no other modifications in metabolic hormones. In contrast, treatment with the leptin antagonist on PND 9 did not affect food intake but reduced body weight beginning around PND 60 (P < 0.02). This was associated with a reduction in fat mass, insulin (P < 0.01), and leptin (P < 0.007) levels and an increase in testosterone levels (P < 0.01). Hypothalamic neuropeptide Y (P < 0.05) and leptin receptor (P < 0.005) mRNA levels were reduced, whereas mRNA levels for uncoupling protein 2 (P < 0.005) were increased in visceral fat, which may indicate an increase in energy expenditure. In conclusion, acute changes in neonatal leptin levels induce different metabolic profiles depending on how and when leptin levels are modified.

Comparison of Long-Term Care Residents' Food Intake, Body Weight, and Food Costs between Two Meal Service Styles

2009 ◽  
Vol 109 (9) ◽  
pp. A65
Author(s):  
D.R. Murphy ◽  
J.T. Brooks ◽  
A.J. Rainville
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Long Term Care ◽  
Term Care ◽  
Meal Service

scholarly journals Antiobesity Effects of the β-Cell Hormone Amylin in Diet-Induced Obese Rats: Effects on Food Intake, Body Weight, Composition, Energy Expenditure, and Gene Expression

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5855-5864 ◽  
Author(s):  
Jonathan D. Roth ◽  
Heather Hughes ◽  
Eric Kendall ◽  
Alain D. Baron ◽  
Christen M. Anderson
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Respiratory Quotient ◽  
Metabolic Effects ◽  
Mrna Levels ◽  
Lean Tissue ◽  
Reduced Body ◽  
Diet Induced Obesity ◽  
Cell Hormone

Effects of amylin and pair feeding (PF) on body weight and metabolic parameters were characterized in diet-induced obesity-prone rats. Peripherally administered rat amylin (300 μg/kg·d, 22d) reduced food intake and slowed weight gain: approximately 10% (P < 0.05), similar to PF. Fat loss was 3-fold greater in amylin-treated rats vs. PF (P < 0.05). Whereas PF decreased lean tissue (P < 0.05 vs. vehicle controls; VEH), amylin did not. During wk 1, amylin and PF reduced 24-h respiratory quotient (mean ± se, 0.82 ± 0.0, 0.81 ± 0.0, respectively; P < 0.05) similar to VEH (0.84 ± 0.01). Energy expenditure (EE mean ± se) tended to be reduced by PF (5.67 ± 0.1 kcal/h·kg) and maintained by amylin (5.86 ± 0.1 kcal/h·kg) relative to VEH (5.77 ± 0.0 kcal/h·kg). By wk 3, respiratory quotient no longer differed; however, EE increased with amylin treatment (5.74 ± 0.09 kcal/·kg; P < 0.05) relative to VEH (5.49 ± 0.06) and PF (5.38 ± 0.07 kcal/h·kg). Differences in EE, attributed to differences in lean mass, argued against specific amylin-induced thermogenesis. Weight loss in amylin and pair-fed rats was accompanied by similar increases arcuate neuropeptide Y mRNA (P < 0.05). Amylin treatment, but not PF, increased proopiomelanocortin mRNA levels (P < 0.05 vs. VEH). In a rodent model of obesity, amylin reduced body weight and body fat, with relative preservation of lean tissue, through anorexigenic and specific metabolic effects.

Pulmonary delivery of peptide YY for food intake suppression and reduced body weight gain in rats

2011 ◽  
Vol 13 (5) ◽  
pp. 408-417 ◽  
Author(s):  
P. P. Nadkarni ◽  
R. M. Costanzo ◽  
M. Sakagami
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Peptide Yy ◽  
Body Weight Gain ◽  
Pulmonary Delivery ◽  
Reduced Body

scholarly journals Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight

2008 ◽  
Vol 88 (4) ◽  
pp. 906-912 ◽  
Author(s):  
Michael Rosenbaum ◽  
Jules Hirsch ◽  
Dympna A Gallagher ◽  
Rudolph L Leibel
Keyword(s):  
Body Weight ◽  
Adaptive Thermogenesis ◽  
Reduced Body

Long-term effects of TRH administration on food intake and body weight in the rat

1986 ◽  
Vol 24 (6) ◽  
pp. 1817-1819 ◽  
Author(s):  
R. Iglesias ◽  
M. Llobera ◽  
E. Montoya
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Long Term Effects

scholarly journals Hindbrain administration of NMDA receptor antagonist AP-5 increases food intake in the rat

2006 ◽  
Vol 290 (3) ◽  
pp. R642-R651 ◽  
Author(s):  
Chun-Yi Hung ◽  
M. Covasa ◽  
R. C. Ritter ◽  
G. A. Burns
Keyword(s):  
Nmda Receptor ◽  
Food Intake ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Intraperitoneal Injection ◽  
Sucrose Solution ◽  
Nmda Receptor Antagonist ◽  
Saline Control ◽  
Sucrose Intake ◽  
Mk 801

Hindbrain administration of MK-801, a noncompetitive N-methyl-d-aspartate (NMDA) channel blocker, increases meal size, suggesting NMDA receptors in this location participate in control of food intake. However, dizocilpine (MK-801) reportedly antagonizes some non-NMDA ion channels. Therefore, to further assess hindbrain NMDA receptor participation in food intake control, we measured deprivation-induced intakes of 15% sucrose solution or rat chow after intraperitoneal injection of either saline vehicle or d(-)-2-amino-5-phosphonopentanoic acid (AP5), a competitive NMDA receptor antagonist, to the fourth ventricular, or nucleus of the solitary tract (NTS). Intraperitoneal injection of AP5 (0.05, 0.1, 1.0, 3.0, and 5.0 mg/kg) did not alter 30-min sucrose intake at any dose (10.7 ± 0.4 ml, saline control) (11.0 ± 0.8, 11.2 ± 1.0, 11.2 ± 1.0, 13.1 ± 2.2, and 11.0 ± 1.9 ml, AP5 doses, respectively). Fourth ventricular administration of both 0.2 μg (16.7 ± 0.6 ml) and 0.4 μg (14.9 ± 0.5 ml) but not 0.1 and 0.6 μg of AP5 significantly increased 60-min sucrose intake compared with saline (11.2 ± 0.4 ml). Twenty-four hour chow intake also was increased compared with saline (AP5: 31.5 ± 0.1 g vs. saline: 27.1 ± 0.6 g). Furthermore, rats did not increase intake of 0.2% saccharin after fourth ventricular AP5 administration (AP5: 9.8 ± 0.7ml, vs. saline: 10.5 ± 0.5ml). Finally, NTS AP5 (20 ng/30 nl) significantly increased 30- (AP5: 17.2 ± 0.7 ml vs. saline: 14.6 ± 1.7 ml), and 60-min (AP5: 19.4 ± 0.6 ml vs. saline: 15.5 ± 1.4 ml) sucrose intake, as well as 24-h chow intake (AP5: 31.6 ± 0.3 g vs. saline: 26.1 ± 1.2 g). These results support the hypothesis that hindbrain NMDA receptors participate in control of food intake and suggest that this participation also may contribute to control of body weight over a 24-h period.

Experimental chronic subdural hematoma in mice

1987 ◽  
Vol 67 (5) ◽  
pp. 710-716 ◽  
Author(s):  
Hisashi Aikawa ◽  
Kinuko Suzuki
Keyword(s):  
Body Weight ◽  
Blood Vessels ◽  
Subdural Hematoma ◽  
Intraperitoneal Injection ◽  
Intraventricular Hemorrhage ◽  
Chronic Subdural Hematoma ◽  
Content Type ◽  
Single Intraperitoneal Injection ◽  
Thin Walled ◽  
Fine Print

✓ A new experimental model of chronic subdural hematoma in mice is described. A single intraperitoneal injection of 6-aminonicotinamide (25 mg/kg body weight) on the 5th postnatal day induced hydrocephalus in mice with almost 100% success. Approximately 60% of the mice spontaneously developed intracranial hemorrhage 20 days after the injection. About 1 week after the hemorrhage, a lens-shaped or spherical subdural hematoma was observed, accompanied by marked dilatation of the lateral ventricles and intraventricular hemorrhage. Histological examination revealed that the hematoma contained well-organized outer and inner membranes. Fresh hemorrhage surrounded by many hemosiderin-laden macrophages was seen at the margin of the hematoma adjacent to the organizing outer membrane, in which many fibroblasts and blood vessels were noted. The inner membrane of the hematoma was made up of several tiers of flattened cells with thin-walled blood vessels. The gross morphology and histology of these hematomas closely resembled those of human chronic subdural hematoma.

Glucocorticoids and insulin: reciprocal signals for energy balance

1995 ◽  
Vol 268 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
A. M. Strack ◽  
R. J. Sebastian ◽  
M. W. Schwartz ◽  
M. F. Dallman
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Diabetic Rats ◽  
Energy Gain ◽  
Energy Stores ◽  
The Central Nervous System ◽  
Streptozotocin Induced Diabetes ◽  
Term Energy

Signals that regulate long-term energy balance have been difficult to identify. Increasingly strong evidence indicates that insulin, acting on the central nervous system in part through its effect on neuropeptide Y (NPY), inhibits food intake. We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores. Because glucocorticoids also stimulate insulin secretion, their role is normally obscured. Glucocorticoids and insulin were clamped in adrenalectomized rats with steroid replacement and streptozotocin-induced diabetes. Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake. Glucocorticoids inhibited and insulin increased energy gain as determined by the change in body weight. When adrenalectomized diabetic rats were treated, corticosterone stimulated and insulin inhibited food intake, and, respectively, inhibited and increased overall energy gain. More than 50% of the variance was explained by regression analysis of the two hormones on food intake and body weight. Thus glucocorticoids and insulin are major, antagonistic, long-term regulators of energy balance. The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.

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