Effects of duodenal and distal ileal infusions of glucose and oleic acid on meal patterns in rats

1995 ◽  
Vol 269 (1) ◽  
pp. R7-R14 ◽  
Author(s):  
T. Woltman ◽  
R. Reidelberger
Keyword(s):  
Oleic Acid ◽  
Dark Period ◽  
Meal Size ◽  
Meal Frequency ◽  
Meal Patterns ◽  
Distal Small Intestine ◽  
Ad Libitum ◽  
Dose Dependent ◽  
Ad Libitum Feeding ◽  
Cumulative Food Intake

The mechanisms mediating the anorexic effects of nutrients in the proximal and distal small intestine are not clearly understood. We determined the dose-dependent effects of duodenal and distal ileal infusions of glucose and oleic acid on meal patterns in ad libitum feeding rats. Rats with cannulas in both the duodenum and ileum received a 2-h infusion of glucose (0, 800, 1,600, 3,200, 6,400, or 12,800 mumol/h) or oleic acid (0, 48, 240, 640, or 1,280 mumol/h) into the duodenum or ileum at the start of the dark period, and meal patterns were monitored for 4 h. Cumulative food intake was inhibited dose dependently by ileal as well as duodenal infusion of both glucose and oleic acid. Ileal glucose was more inhibitory than duodenal glucose, whereas duodenal oleic acid was more inhibitory than ileal oleic acid. Duodenal glucose and oleic acid inhibited feeding by decreasing meal frequency; ileal oleic acid decreased only meal size, whereas ileal glucose reduced both meal size and frequency. We interpret these results to suggest that ileal oleic acid and glucose suppress feeding by different mechanisms and that these mechanisms differ from those mediating the anorexic responses to oleic acid and glucose in the duodenum.

Mode of action of OB protein (leptin) on feeding

1998 ◽  
Vol 275 (1) ◽  
pp. R174-R179 ◽  
Author(s):  
Mark C. Flynn ◽  
Thomas R. Scott ◽  
Thomas C. Pritchard ◽  
Carlos R. Plata-Salamán
Keyword(s):  
Food Intake ◽  
Wistar Rats ◽  
Feeding Rate ◽  
Meal Size ◽  
Meal Frequency ◽  
Dependent Manner ◽  
Intracerebroventricular Administration ◽  
Ad Libitum ◽  
Ob Protein ◽  
Dose Dependent

OB protein (leptin) decreases food intake in a variety of species. Here we investigated the effects of the intracerebroventricular administration of recombinant murine OB protein on food consumption and meal parameters in Wistar rats maintained ad libitum. The intracerebroventricular administration of OB protein (0.56–3.5 μg/rat) decreased feeding in a dose-dependent manner. Computer analysis of meal parameters demonstrated that OB protein (3.5 μg/rat, n = 10) decreased nighttime meal size by 42%, whereas meal frequency and meal duration were unaffected. Derived analyses for the nighttime also showed that OB protein decreased the feeding rate (meal size/meal duration) by 30%, whereas the satiety ratio (intermeal intervals/meal size) increased by 100%. A similar profile was observed during the daytime and total daily periods. The intracerebroventricular administration of heat-inactivated OB protein (3.5 μg/rat, n = 10) had no effect on any meal parameter. The results show that OB protein administered intracerebroventricularly inhibits feeding through a specific reduction of meal size.

scholarly journals Role of cholecystokinin in the anorexia produced by duodenal delivery of oleic acid in rats

1995 ◽  
Vol 269 (6) ◽  
pp. R1420-R1433 ◽  
Author(s):  
T. Woltman ◽  
D. Castellanos ◽  
R. Reidelberger
Keyword(s):  
Oleic Acid ◽  
Receptor Antagonist ◽  
Type A ◽  
Meal Patterns ◽  
Cholecystokinin Octapeptide ◽  
Satiety Response ◽  
Ad Libitum ◽  
Ad Libitum Feeding

To assess the importance of triglyceride digestion products in producing satiety, we determined the effects of duodenal infusions of triolein, oleic acid, and oleic acid plus monoolein on meal patterns in ad libitum-feeding rats. Oleic acid and oleic acid plus monoolein inhibited feeding similarly; triolein's effect was delayed and fourfold less potent. We then used the type A cholecystokinin (CCK-A)-receptor antagonist devazepide to assess the importance of CCK in mediating the anorexia produced by oleic acid. Oleic acid (at 320, 440, and 640 mumol/h) inhibited 3-h intake dose dependently by 32, 56, and 75%, respectively. Devazepide (1 or 2 mg/kg) blocked the responses to the 320 mumol/h dose, but had little if any effect on responses to the larger doses. Devazepide (1 mg/kg) did block anorexic responses to 3-h cholecystokinin octapeptide infusions (3 and 10 nmol.kg-1.h-1 iv) that inhibited 3-h intake by 25 and 65%, respectively. Our results suggest that the satiety response to triolein is produced by the products of triolein digestion and that CCK plays a significant, indispensable role in mediating the satiety response to duodenal delivery of small but not large loads of oleic acid.

Effect of food manipulation on the GnRH-LH-estradiol axis of young female rats

1988 ◽  
Vol 254 (4) ◽  
pp. R616-R621 ◽  
Author(s):  
F. H. Bronson
Keyword(s):  
Food Restriction ◽  
Dark Period ◽  
Pubertal Development ◽  
Young Female ◽  
Female Rats ◽  
The Third ◽  
Feedback Sensitivity ◽  
Effect Of Food ◽  
Ad Libitum ◽  
Ad Libitum Feeding

Female rats were prevented from growing and developing reproductively by restricting their food intake from the time they reached 80-85 g (27-29 days of age) until they were 2 mo old. A return to ad libitum feeding then typically yielded the pubertal ovulation during the third or fourth dark period. Ad libitum feeding for 48 h increased the frequency of luteinizing hormone (LH) pulsing in ovariectomized females. This treatment also depressed the level of circulating estradiol in ovariectomized females implanted with Silastic capsules. It had no effect on the rate at which estradiol was cleared from the blood in a 1-h test, however, nor did it affect the pool of assayable gonadotropin-releasing hormone (GnRH) in the hypothalamus, the pool of assayable LH in the pituitary, the response of the pituitary to GnRH, or the rate at which LH was cleared from the blood. In toto, the present results suggest that food restriction inhibits pubertal development by acting rather specifically on GnRH secretion via an ovarian steroid-independent pathway. The presumed supplemental role for enhanced negative-feedback sensitivity could not be evaluated because of the aberrant results with encapsulated estradiol.

scholarly journals Blood glucose and meal patterns in time-blinded males, after aspartame, carbohydrate, and fat consumption, in relation to sweetness perception

1999 ◽  
Vol 82 (6) ◽  
pp. 437-446 ◽  
Author(s):  
Kathleen J. Melanson ◽  
Margriet S. Westerterp-Plantenga ◽  
L. Arthur Campfield ◽  
Wim H. M. Saris
Keyword(s):  
Blood Glucose ◽  
Meal Size ◽  
High Fat ◽  
Meal Patterns ◽  
High Carbohydrate ◽  
Fat Consumption ◽  
Ad Libitum ◽  
The Impact ◽  
Simple Carbohydrate ◽  
Healthy Males

In a study of the impact of aspartame, fat, and carbohydrate on appetite, we monitored blood glucose continuously for 431 (se 16) min. Ten healthy males (19–31 years) participated in three time-blinded visits. As blood glucose was monitored, appetite ratings were scored at randomized times. On the first meal initiation, volunteers consumed one of three isovolumetric drinks (aspartame, 1 MJ simple carbohydrate, and 1 MJ high-fat; randomized order). High-fat and high-carbohydrate foods were available ad libitum subsequently. Blood glucose patterns following the carbohydrate drink (+1·78 (se 0·28) mmol/l in 38 (se 3) min) and high-fat drink (+0·83 (se 0·28) mmol/l in 49 (se 6) min) were predictive of the next intermeal interval (R 0·64 and R 0·97 respectively). Aspartame ingestion was followed by blood glucose declines (40 % of subjects), increases (20 %), or stability (40 %). These patterns were related to the volunteers' perception of sweetness of the drink (R 0·81, P = 0·014), and were predictive of subsequent intakes (R -0·71, P = 0·048). For all drinks combined, declines in blood glucose and meal initiation were significantly associated (χ2 16·8, P < 0·001), the duration of blood glucose responses and intermeal intervals correlated significantly (R 0·715, P = 0·0001), and sweetness perception correlated negatively with hunger suppression (R -0·471, P = 0·015). Effects of fat, carbohydrate, and aspartame on meal initiation, meal size, and intermeal interval relate to blood glucose patterns. Varied blood glucose responses after aspartame support the controversy over its effects, and may relate to sweetness perception.

scholarly journals Effect of dietary fructose on portal and systemic serum fructose levels in rats and in KHK−/− and GLUT5−/− mice

2015 ◽  
Vol 309 (9) ◽  
pp. G779-G790 ◽  
Author(s):  
Chirag Patel ◽  
Keiichiro Sugimoto ◽  
Veronique Douard ◽  
Ami Shah ◽  
Hiroshi Inui ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Organ Dysfunction ◽  
Elevated Blood ◽  
Wild Type ◽  
Dietary Fructose ◽  
Ad Libitum ◽  
Induced Changes ◽  
Dose Dependent ◽  
Ad Libitum Feeding ◽  
Endogenous Synthesis

Elevated blood fructose concentrations constitute the basis for organ dysfunction in fructose-induced metabolic syndrome. We hypothesized that diet-induced changes in blood fructose concentrations are regulated by ketohexokinase (KHK) and the fructose transporter GLUT5. Portal and systemic fructose concentrations determined by HPLC in wild-type mice fed for 7 days 0% free fructose were <0.07 mM, were independent of time after feeding, were similar to those of GLUT5−/−, and did not lead to hyperglycemia. Postprandial fructose levels, however, increased markedly in those fed isocaloric 20% fructose, causing significant hyperglycemia. Deletion of KHK prevented fructose-induced hyperglycemia, but caused dramatic hyperfructosemia (>1 mM) with reversed portal to systemic gradients. Systemic fructose in wild-type and KHK−/− mice changed by 0.34 and 1.8 mM, respectively, for every millimolar increase in portal fructose concentration. Systemic glucose varied strongly with systemic, but not portal, fructose levels in wild-type, and was independent of systemic and portal fructose in KHK−/−, mice. With ad libitum feeding for 12 wk, fructose-induced hyperglycemia in wild-type, but not hyperfructosemia in KHK−/− mice, increased HbA1c concentrations. Increasing dietary fructose to 40% intensified the hyperfructosemia of KHK−/− and the fructose-induced hyperglycemia of wild-type mice. Fructose perfusion or feeding in rats also caused duration- and dose-dependent hyperfructosemia and hyperglycemia. Significant levels of blood fructose are maintained independent of dietary fructose, KHK, and GLUT5, probably by endogenous synthesis of fructose. KHK prevents hyperfructosemia and fructose-induced hyperglycemia that would markedly increase HbA1c levels. These findings explain the hyperfructosemia of human hereditary fructosuria as well as the hyperglycemia of fructose-induced metabolic syndrome.

Prefeeding increase in paraventricular NE release is regulated by a feeding-associated rhythm in rats

1994 ◽  
Vol 266 (4) ◽  
pp. E606-E611
Author(s):  
M. Mitome ◽  
S. Honma ◽  
T. Yoshihara ◽  
K. Honma
Keyword(s):  
Food Deprivation ◽  
Dark Period ◽  
Fixed Time ◽  
Plasma Corticosterone ◽  
In Vivo Microdialysis ◽  
Time Of Day ◽  
Daily Feeding ◽  
Ad Libitum ◽  
Ad Libitum Feeding

Extracellular norepinephrine (NE) in the vicinity of the paraventricular nucleus was continuously measured over 24 h by means of in vivo microdialysis in rats under restricted daily feeding and ad libitum feeding. A 24-h rhythm in plasma corticosterone was monitored in separate rats under identical conditions. Under ad libitum feeding, the paraventricular NE showed a 24-h rhythm with lower levels in the light period and higher levels in the dark period. The temporal pattern was not affected by food deprivation for 3 days. The circadian peak of paraventricular NE lagged slightly behind that of plasma corticosterone under ad libitum feeding. On the other hand, when rats were fed for 2 h at a fixed time of day for 3 wk, the NE rhythm was changed and showed a major peak just before daily meals. To examine the nature of the prefeeding NE peak, a 24-hour variation of paraventricular NE was measured in rats under food deprivation that had been subjected to restricted daily feeding for 3 wk and subsequently to ad libitum feeding for 7 days. The paraventricular NE was high around the time when meal had been supplied under restricted daily feeding and low in the dark period. Similar changes were observed in plasma corticosterone. The findings indicate that the prefeeding increase in the paraventricular NE release is regulated by a feeding-associated circadian rhythm manifest in rats under restricted daily feeding.

Diurnal variation of intensive running in food-deprived rats

1995 ◽  
Vol 73 (10) ◽  
pp. 1519-1523 ◽  
Author(s):  
Allen D. Morse ◽  
James C. Russell ◽  
Terry W. M. Hunt ◽  
George O. Wood ◽  
W. Frank Epling ◽  
...  
Keyword(s):  
Diurnal Variation ◽  
Wheel Running ◽  
Dark Period ◽  
Male Rats ◽  
Diurnal Pattern ◽  
Daily Cycle ◽  
Rate Of Increase ◽  
Ad Libitum ◽  
Ad Libitum Feeding ◽  
Day By Day

Manipulation of the food supply can induce either intense hyperactive wheel running or a fatal activity anorexia in rats that is strongly analogous to that seen in humans. The abnormal behaviour is accompanied by alterations in the diurnal pattern of activity. As part of a detailed study of hyperactivity and anorexia, spontaneous wheel running by male rats was studied under three conditions: ad libitum feeding; restriction to 15 g of food per day; and restriction to a single 90-min meal per day. Ad libitum fed rats increased their running at the rate of 440 ± 60 m/day per day, stabilizing after day 10 at 6045 ± 3010 m/day. The running occurred in short bursts throughout the dark period and at the beginning of the light period. Rats restricted to 15 g/day increased their running at the significantly greater (p < 0.001) rate of 1230 ± 120 m/day per day, reaching 12 200 ± 4090 m/day by day 10 and thereafter stabilizing at 13 600 ± 4 160 m/day. The running was initially triphasic and confined to the dark period but eventually progressed to a biphasic pattern. The rats restricted to a single 90-min access period to food each day showed an even greater rate of increase in running, attaining 1930 ± 288 m/day per day (p < 0.02 vs. 15 g/day group). These animals decreased eating and decompensated by day 4. The diurnal pattern of activity was disturbed from day 1 of the protocol, and by day 4 the rats ran essentially continuously throughout the daily cycle. The sensitivity to hyperactivity is a function of the severity of food restriction in this animal model of hyperactivity. It is paralleled by a marked disturbance of the diurnal pattern of activity, suggesting that the hyperactivity is related to a basic central nervous system dysfunction.Key words: hyperactivity, diurnal variation, rat.

Prolactin stimulates food intake in a dose-dependent manner

1989 ◽  
Vol 256 (1) ◽  
pp. R276-R280 ◽  
Author(s):  
T. Gerardo-Gettens ◽  
B. J. Moore ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Food Intake ◽  
Female Rats ◽  
High Dose ◽  
Dependent Manner ◽  
Additional Control ◽  
The Mean ◽  
Ovine Prolactin ◽  
Dose Dependent ◽  
Medium Dose ◽  
Cumulative Food Intake

Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Selection for components of efficient lean growth rate in pigs 2. Selection pressure applied and direct responses in a Landrace herd

1994 ◽  
Vol 59 (2) ◽  
pp. 263-269 ◽  
Author(s):  
N. D. Cameron ◽  
M. K. Curran
Keyword(s):  
Growth Rate ◽  
Genetic Correlations ◽  
Correlated Response ◽  
Selection Line ◽  
Control Line ◽  
Direct Response ◽  
Lean Growth ◽  
Ad Libitum ◽  
Selection For ◽  
Ad Libitum Feeding

AbstractResponses to divergent selection for lean growth rate with ad-libitum feeding (LGA), for lean food conversion (LFC) and for daily food intake (DFI) in Landrace pigs were studied. Selection was practised for four generations with a generation interval ofl year. A total of 2642 pigs were performance tested in the high, low and control lines, with an average of 37 boars and 39 gilts performance tested per selection line in each generation. The average within-line inbreeding coefficient at generation four was equal to 0·04. There was one control line for the DFI and LFC selection groups and another control line for the LGA selection group. Animals were performance tested in individual pens with mean starting and finishing weights of 30 kg and 85 kg respectively with ad-libitum feeding. The selection criteria had phenotypic s.d. of 32, 29 and 274 units, for LGA, LFC and DFI, respectively, and results are presented in phenotypic s.d.Cumulative selection differentials (CSD) were 5·1, 4·5 and 5·5 phenotypic s.d. for LGA, LFC and DFI, respectively. Direct responses to selection were 1·4,1·1 and 0·9 (s.e. 0·20) for LGA, LFC and DFI. In each of the three selection groups, the CSD and direct responses to selection were symmetric about the control lines. The correlated response in LFC (1·1, s.e. 0·19) with selection on LGA was equal to the direct response in LFC. In contrast, the direct response in LGA was greater than the correlated response (0·7, s.e. 0·18) with selection on LFC. There was a negative correlated response in DFI (-0·6, s.e. 0·18) with selection on LFC, but the response with selection on LGA was not significant (0·2, s.e. 0·16).Heritabilities for LGA, LFC and DFI ivere 0·25, 0·25 and 0·18 (s.e. 0·03), when estimated by residual maximum likelihood, with common environmental effects of 0·12 (s.e. 0·02). Genetic correlations for LFC with LGA and DFI were respectively positive (0·87, s.e. 0·02) and negative (-0·36, s.e. 0·09), while the genetic correlation between DFI and LGA was not statistically different from zero, 0·13 (s.e. 0·10). Selection on components of efficient lean growth has identified LGA as an effective selection objective for improving both LGA and LFC, without a reduction in DFI.

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