The effect of ambient temperature on rectal temperature, food intake and short term body weight in the capsaicin desensitized rat

1981 ◽  
Vol 389 (2) ◽  
pp. 171-174 ◽  
Author(s):  
M. Cormar�che-Leydier
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Ambient Temperature ◽  
Rectal Temperature ◽  
Short Term

Effect of Changes in Ambient Temperature on Spontaneous Activity, Food Intake and Body Weight of Goldthioglucose-Obese and Nonobese Mice

1957 ◽  
Vol 188 (3) ◽  
pp. 435-438 ◽  
Author(s):  
M. J. Fregly ◽  
N. B. Marshall ◽  
J. Mayer
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Ambient Temperature ◽  
The Body ◽  
Lower Body ◽  
Obese Mice ◽  
Ambient Temperatures ◽  
Exposure To Cold ◽  
Running Activity ◽  
Body Weights

Goldthioglucose-obese mice cannot adjust their food intake to meet the increased energy requirements due to cold. At all ambient temperatures above 15°C the spontaneous running activity of these animals is less than that observed for nonobese controls. Activity of obese mice is maximal at 19°C and minimal at 15°C or lower. Body weights decrease during exposure to cold. In contrast to that of obese mice, running activity of nonobese controls is maximal at an ambient temperature of 25°C but nearly ceases at 15°C or lower. The food intake of these animals increases in the cold and remains elevated even at temperatures at which activity decreases. The body weight of nonobese controls is either maintained constant or increases during exposure to cold air.

Cholecystokinin reduces body temperature in vehicle- but not capsaicin-pretreated rats

1992 ◽  
Vol 263 (6) ◽  
pp. R1215-R1221 ◽  
Author(s):  
E. H. South
Keyword(s):  
Food Intake ◽  
Body Temperature ◽  
Ambient Temperature ◽  
Rectal Temperature ◽  
Neural Substrates ◽  
Systemic Administration ◽  
Capsaicin Application ◽  
Presence And Absence ◽  
Sensory Fibers ◽  
Maximal Suppression

Systemic administration of cholecystokinin C-terminal octapeptide (CCK-8) decreases body temperature. However, it remains unclear whether reduction of body temperature is concomitant with suppression of food intake at CCK-8 doses that approach physiological levels. We examined rectal temperature after intraperitoneal CCK-8, 4 micrograms/kg, both in the presence and absence of a preferred food. We found that rectal temperature was significantly reduced by CCK-8 in both conditions and that the reduction of temperature coincided with the time of maximal suppression of food intake by CCK-8. In rats pretreated systemically with 25 or 175 mg/kg of the sensory neurotoxin capsaicin, both suppression of food intake and reduction of body temperature were significantly attenuated or abolished. The 25 mg/kg capsaicin treatment did not alter corneal chemosensitivity or the ability of rats to maintain normothermia at elevated ambient temperature, suggesting that capsaicin damage to neural substrates mediating CCK-8-induced reduction of body temperature 1) did not generalize to cephalic or peripheral warm-sensitive structures, and 2) was limited to fine sensory fibers accessible to intraperitoneal capsaicin application.

scholarly journals Oxytocin Administration Alleviates Acute but Not Chronic Leptin Resistance of Diet-Induced Obese Mice

2018 ◽  
Vol 20 (1) ◽  
pp. 88 ◽  
Author(s):  
Mehdi Labyb ◽  
Chloé Chrétien ◽  
Aurélie Caillon ◽  
Françoise Rohner-Jeanrenaud ◽  
Jordi Altirriba
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Leptin Resistance ◽  
Obese Mice ◽  
Short Term ◽  
Continuous Administration ◽  
Pre Treatment ◽  
Treatment Of Obesity

Whereas leptin administration only has a negligible effect on the treatment of obesity, it has been demonstrated that its action can be improved by co-administration of leptin and one of its sensitizers. Considering that oxytocin treatment decreases body weight in obese animals and humans, we investigated the effects of oxytocin and leptin cotreatment. First, lean and diet-induced obese (DIO) mice were treated with oxytocin for 2 weeks and we measured the acute leptin response. Second, DIO mice were treated for 2 weeks with saline, oxytocin (50 μg/day), leptin (20 or 40 µg/day) or oxytocin plus leptin. Oxytocin pre-treatment restored a normal acute leptin response, decreasing food intake and body weight gain. Chronic continuous administration of oxytocin or leptin at 40 µg/day decreased body weight in the presence (leptin) or in the absence (oxytocin) of cumulative differences in food intake. Saline or leptin treatment at 20 µg/day had no impact on body weight. Oxytocin and leptin cotreatments had no additional effects compared with single treatments. These results point to the fact that chronic oxytocin treatment improves the acute, but not the chronic leptin response, suggesting that this treatment could be used to improve the short-term satiety effect of leptin.

scholarly journals Combination Therapy with Amylin and Peptide YY[3–36] in Obese Rodents: Anorexigenic Synergy and Weight Loss Additivity

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 6054-6061 ◽  
Author(s):  
Jonathan D. Roth ◽  
Todd Coffey ◽  
Carolyn M. Jodka ◽  
Holly Maier ◽  
Jennifer R. Athanacio ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Peptide Yy ◽  
Peptide Hormone ◽  
Short Term ◽  
Subcutaneous Infusion ◽  
Body Weight Reduction ◽  
Diet Induced Obesity ◽  
Circulating Levels

Circulating levels of the pancreatic β-cell peptide hormone amylin and the gut peptide PYY[3–36] increase after nutrient ingestion. Both have been implicated as short-term signals of meal termination with anorexigenic and weight-reducing effects. However, their combined effects are unknown. We report that the combination of amylin and PYY[3–36] elicited greater anorexigenic and weight-reducing effects than either peptide alone. In high-fat-fed rats, a single ip injection of amylin (10 μg/kg) plus PYY[3–36] (1000 μg/kg) reduced food intake for 24 h (P < 0.05 vs. vehicle), whereas the anorexigenic effects of either PYY[3–36] or amylin alone began to diminish 6 h after injection. These anorexigenic effects were dissociable from changes in locomotor activity. Subcutaneous infusion of amylin plus PYY[3–36] for 14 d suppressed food intake and body weight to a greater extent than either agent alone in both rat and mouse diet-induced obesity (DIO) models (P < 0.05). In DIO-prone rats, 24-h metabolic rate was maintained despite weight loss, and amylin plus PYY[3–36] (but not monotherapy) increased 24-h fat oxidation (P < 0.05 vs. vehicle). Finally, a 4 × 3 factorial design was used to formally describe the interaction between amylin and PYY[3–36]. DIO-prone rats were treated with amylin (0, 4, 20, and 100 μg/kg·d) and PYY[3–36] (0, 200, 400 μg/kg·d) alone and in combination for 14 d. Statistical analyses revealed that food intake suppression with amylin plus PYY[3–36] treatment was synergistic, whereas body weight reduction was additive. Collectively, these observations highlight the importance of studying peptide hormones in combination and suggest that integrated neurohormonal approaches may hold promise as treatments for obesity.

scholarly journals Pancreatic signals controlling food intake; insulin, glucagon and amylin

2006 ◽  
Vol 361 (1471) ◽  
pp. 1219-1235 ◽  
Author(s):  
Stephen C Woods ◽  
Thomas A Lutz ◽  
Nori Geary ◽  
Wolfgang Langhans
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Endocrine Pancreas ◽  
Situational Factors ◽  
Meal Size ◽  
Vagus Nerves ◽  
Social Emotional ◽  
Short Term ◽  
The Brain

The control of food intake and body weight by the brain relies upon the detection and integration of signals reflecting energy stores and fluxes, and their interaction with many different inputs related to food palatability and gastrointestinal handling as well as social, emotional, circadian, habitual and other situational factors. This review focuses upon the role of hormones secreted by the endocrine pancreas: hormones, which individually and collectively influence food intake, with an emphasis upon insulin, glucagon and amylin. Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue. Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight. Amylin reduces meal size by stimulating neurons in the hindbrain, and there is evidence that amylin additionally functions as an adiposity signal controlling body weight as well as meal size. Glucagon is secreted from A-cells and increases glucose secretion from the liver. Glucagon acts in the liver to reduce meal size, the signal being relayed to the brain via the vagus nerves. To summarize, hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis. Glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amylin as well act over longer intervals to modulate the amount of fat maintained and defended by the brain. Hormones of the endocrine pancreas interact with receptors at many points along the gut–brain axis, from the liver to the sensory vagus nerve to the hindbrain to the hypothalamus; and their signals are conveyed both neurally and humorally. Finally, their actions include gastrointestinal and metabolic as well as behavioural effects.

Increased short-term food satiation and sensitivity to cholecystokinin in neurotrophin-4 knock-in mice

2004 ◽  
Vol 287 (5) ◽  
pp. R1044-R1053 ◽  
Author(s):  
Michael M. Chi ◽  
Guoping Fan ◽  
Edward A. Fox
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Knockout Mice ◽  
Meal Frequency ◽  
Short Term ◽  
Daily Food Intake ◽  
Food Satiation ◽  
Daily Food ◽  
Solid Diet

Neurotrophin-4 (NT-4) knockout mice exhibited decreased innervation of the small intestine by vagal intraganglionic laminar endings (IGLEs) and reduced food satiation. Recent findings suggested this innervation was increased in NT-4 knock-in (NT-4KI) mice. Therefore, to further investigate the relationship between intestinal IGLEs and satiation, meal patterns were characterized using solid and liquid diets, and cholecystokinin (CCK) effects on 30-min solid diet intake were examined in NT-4KI and wild-type mice. NT-4KI mice consuming the solid diet exhibited reduced meal size, suggesting increased satiation. However, compensation occurred through increased meal frequency, maintaining daily food intake and body weight gain similar to controls. Mutants fed the liquid diet displayed a decrease in intake rate, again implying increased satiation, but meal duration increased, which led to an increase in meal size. This was compensated for by decreased meal frequency, resulting in similar daily food intake and weight gain as controls. Importantly, these alterations in NT-4KI mice were opposite, or different, from those of NT-4 knockout mice, further supporting the hypothesis that they are specific to vagal afferent signaling. CCK suppressed short-term intake in mutants and controls, but the mutants exhibited larger suppressions at lower doses, implying they were more sensitive to CCK. Moreover, devazepide prevented this suppression, indicating this increased sensitivity was mediated by CCK-1 receptors. These results suggest that the NT-4 gene knock-in, probably involving increased intestinal IGLE innervation, altered short-term feeding, in particular by enhancing satiation and sensitivity to CCK, whereas long-term control of daily intake and body weight was unaffected.

scholarly journals Effects of dietary fat and carbohydrate on appetite vary depending upon site and structure

2004 ◽  
Vol 92 (S1) ◽  
pp. S23-S26 ◽  
Author(s):  
Stephen French
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Dietary Fat ◽  
Chemical Properties ◽  
Present Review ◽  
Dietary Composition ◽  
Levels Of Processing ◽  
Short Term ◽  
Physico Chemical

The present review summarises the effects of different carbohydrate and fat structures on food intake and appetite and the differences in response at various levels of processing of macronutrients. Several physico-chemical properties of carbohydrate and fat molecules appear to influence the short-term satiating properties. However, long-term substantiation of these findings expressed in terms of food intake or body weight is not currently available. Such studies will be required to make clear recommendations regarding dietary composition to aid satiety.

A note on the adaptability of native and cross-bred sheep to hot summer conditions of semi-arid and arid areas

1982 ◽  
Vol 99 (3) ◽  
pp. 525-528 ◽  
Author(s):  
Manohar Singh ◽  
T. More ◽  
A. K. Rai ◽  
S. A. Karim
Keyword(s):  
Body Weight ◽  
Pulse Rate ◽  
Rectal Temperature ◽  
Short Term ◽  
Progressive Decline ◽  
Short Term Exposure ◽  
Summer Stress ◽  
Blood Potassium ◽  
The Cross ◽  
Moisture Increase

SUMMARYRelative adaptability of Chokla and Rambouillet × Chokla half-breds was compared by observing their responses on exposure to summer stress for 6 days and also under accentuated stress by deprivation of drinking water till the animals lost 30% of their body weight. Responses of both the breed groups were similar on 6 days exposure. Accentuated summer stress resulted in decreased feed intake followed by 15, 26 and 31% loss in body weight on 1st, 2nd and 3rd day of exposure, respectively. Progressive decline in faecal moisture, increase in rectal temperature and decrease in morning respiration rate were also noted in both the breeds while an increase in pulse rate was recorded only in the cross-breds. Increase in respiratory or pulse rate for unit rise in rectal temperature was found to be higher in the cross-breds. On accentuated thermal stress, haematocrit values were higher in the cross-breds and blood potassium concentration was higher in the Chokla while blood glucose decreased in both the groups. Under the conditions of short-term exposure to summer stress the cross-breds maintained homoeothermy as well as the Chokla.

scholarly journals Rhythmic neuronal activities of the rat nucleus of the solitary tract are impaired by short-term high fat diet - implications for daily control of satiety by the brainstem

2021 ◽  
Author(s):  
Lukasz Chrobok ◽  
Jasmin D Klich ◽  
Anna M Sanetra ◽  
Jagoda S Jeczmien-Lazur ◽  
Kamil Pradel ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Circadian Rhythms ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Solitary Tract ◽  
High Fat ◽  
Short Term ◽  
Extrinsic Factors

ABSTRACTTemporal partitioning of daily food intake is crucial for survival and involves the integration of internal circadian states and external influences such as the light-dark cycle and the composition of diet. These intrinsic and extrinsic factors are interdependent with misalignment of circadian rhythms promoting body weight gain, while consumption of a calorie dense diet elevates the risk of obesity and blunts circadian rhythms. Since cardiovascular disease, metabolic disorders, and cancer are comorbid with obesity, understanding the relationships between brain activity and diet is of pivotal importance. Recently, we defined for the first time the circadian properties of the dorsal vagal complex of the brainstem, a structure implicated in the control of food intake and autonomic tone, but if and how 24 h rhythms in this area are influenced by diet remains unresolved. Here we focused on a key structure of this complex, the nucleus of the solitary tract, and using a range of approaches, we interrogated how its neuronal and cellular rhythms are affected by high-fat diet. We report that short term consumption of this diet increases food intake during the day and blunts daily rhythms in gene expression and neuronal discharge in the nucleus of the solitary tract. These alterations in this structure occur without prominent body weight gain, suggesting that high-fat diet acts initially to reduce activity in the nucleus of the solitary tract, thereby disinhibiting mechanisms that suppress daytime feeding.GRAPHICAL ABSTRACT

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