Satiating effect of fat in diabetic rats: gastrointestinal and postabsorptive factors

1988 ◽  
Vol 255 (1) ◽  
pp. R123-R127
Author(s):  
N. K. Edens ◽  
M. I. Friedman
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Corn Oil ◽  
Ketone Bodies ◽  
Stomach Contents ◽  
Diabetic Rats ◽  
Physiological Basis ◽  
Streptozotocin Diabetic Rats ◽  
Fat Feeding ◽  
Fat Meal

Streptozotocin-diabetic rats decrease food intake more than normal animals in response to a fat test meal. To determine the physiological basis of this differential response, we examined the effects of an ingested corn oil meal on food intake, gastrointestinal fill, and plasma triglycerides, glycerol, and ketone bodies. Hyperphagic diabetic rats decreased intake of a high-carbohydrate, low-fat stock diet starting 2-4 h after the fat meal, whereas normal rats did not. Gastric emptying was accelerated and intestinal mass and contents were increased in diabetic rats. The fat meal reduced gastric emptying and increased stomach contents in diabetic and normal rats starting within 2 h of ingestion. Intestinal fill decreased in diabetic animals after the oil meal. Triglycerides and glycerol increased transiently after fat ingestion in normal and diabetic rats, whereas ketone body concentrations rose only in diabetic rats starting 1-3 h after fat ingestion. The results indicate that the differential effect of a fat meal on food intake in normal and diabetic rats is related to differences in the postabsorptive metabolism of the ingested fat rather than to effects of fat feeding on gastrointestinal fill or clearance.

Food intake in diabetic rats: isolation of primary metabolic effects of fat feeding

1985 ◽  
Vol 249 (1) ◽  
pp. R44-R51 ◽  
Author(s):  
M. I. Friedman ◽  
I. Ramirez ◽  
N. K. Edens ◽  
J. Granneman
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Metabolic Effects ◽  
Carbohydrate Consumption ◽  
Plasma Triglycerides ◽  
Urinary Glucose ◽  
Ad Libitum ◽  
Fat Feeding

The effects of varying dietary fat content on food intake and metabolism in streptozotocin-diabetic rats were examined. The metabolic consequences of fat feeding were separated from the marked adjustments in voluntary food consumption that occur when diabetic rats are fed diets containing different amounts of fat by feeding rats a fixed ration of food in which either fats or carbohydrates were reduced by equicaloric amounts, or in which only the concentration of fat, but not other dietary nutrients, was varied systematically. Resulting changes in metabolism and subsequent ad libitum food intake on refeeding were then measured. Rats did not increase their food intake after a prior reduction in carbohydrate consumption but did so after an equicaloric reduction in fat consumption. Urinary glucose excretion during rationing was a function of carbohydrate consumption and was not predictive of changes in food intake during refeeding. The more fat that rats consumed during rationing, the higher their levels of plasma triglycerides and ketone bodies were at the time of refeeding and the less they ate when allowed to eat ad libitum. The orderly changes in food consumption and in plasma triglycerides and ketones observed with variations in fat intake suggest that the effects of fat feeding on food intake in diabetic rats are mediated through the oxidation of ingested fat.

Food intake and gastric emptying in rats with streptozotocin-induced diabetes

1984 ◽  
Vol 247 (6) ◽  
pp. R1054-R1061 ◽  
Author(s):  
J. G. Granneman ◽  
E. M. Stricker
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Carbohydrate ◽  
Streptozotocin Induced Diabetes

Recent studies suggest that the rate of nutrient transit through the upper gastrointestract may provide cues that are important to the control of food intake. We examined gastrointestinal function in rats with streptozotocin-induced diabetes and related these findings to concomitant changes in food intake. Control and diabetic rats were adapted to one of two isocaloric diets either high in carbohydrate or fat. Control rats ate similar amounts of each diet. In contrast, diabetic animals fed high-carbohydrate diet were hyperphagic, whereas those fed low-carbohydrate diet ate normal amounts of food. Gastric emptying, intestinal mass, disaccharidase activity, and glucose absorption were increased in normophagic diabetic rats fed a low-carbohydrate diet. Feeding diabetic rats high-carbohydrate diet potentiated each of these effects, and food intake was highly correlated with rate of gastric emptying. These and other results indicate that diabetes enhances gastric emptying and intestinal carbohydrate digestion and absorption, even in the absence of hyperphagia. Consequently, the hyperphagia of diabetic rats may be in part a behavioral response to a greatly accelerated clearance of nutrients from the upper gastrointestinal tract that occurs when these animals are fed diets rich in carbohydrate.

scholarly journals Glutamine and ketone-body metabolism in the gut of streptozotocin-diabetic rats

1988 ◽  
Vol 249 (2) ◽  
pp. 565-572 ◽  
Author(s):  
M S M Ardawi
Keyword(s):  
Small Intestine ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Glutamine Metabolism ◽  
Gut Mucosa ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Short And Long Term

1. In short- and long-term diabetic rats there is a marked increase in size of both the small intestine and colon, which was accompanied by marked decreases (P less than 0.001) and increases (P less than 0.001) in the arterial concentrations of glutamine and ketone bodies respectively. 2. Portal-drained viscera blood flow increased by approx. 14-37% when expressed as ml/100 g body wt., but was approximately unchanged when expressed as ml/g of small intestine of diabetic rats. 3. Arteriovenous-difference measurements for ketone bodies across the gut were markedly increased in diabetic rats, and the gut extracted ketone bodies at approx. 7 and 60 nmol/min per g of small intestine in control and 42-day-diabetic rats respectively. 4. Glutamine was extracted by the gut of control rats at a rate of 49 nmol/min per g of small intestine, which was diminished by 45, 76 and 86% in 7-, 21- and 42-day-diabetic rats respectively. 5. Colonocytes isolated from 7- or 42-day-diabetic rats showed increased and decreased rates of ketone-body and glutamine metabolism respectively, whereas enterocytes of the same animals showed no apparent differences in the rates of acetoacetate utilization as compared with control animals. 6. Prolonged diabetes had no effects on the maximal activities of either glutaminase or ketone-body-utilizing enzymes of colonic tissue preparations. 7. It is concluded that, although the epithelial cells of the small intestine and the colon during streptozotocin-induced diabetes exhibit decreased rates of metabolism of glutamine, such decreases were partially compensated for by enhanced ketone-body utilization by the gut mucosa of diabetic rats.

Does ingested fat produce satiety?

1996 ◽  
Vol 270 (4) ◽  
pp. R761-R765 ◽  
Author(s):  
C. C. Horn ◽  
M. G. Tordoff ◽  
M. I. Friedman
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Feeding Behavior ◽  
Corn Oil ◽  
Substantial Reduction ◽  
Liquid Diet ◽  
Short Term ◽  
Diet Intake ◽  
Marked Suppression ◽  
Fat Meal

Administration of fat directly into the gastrointestinal tract of rats produces a rapid and often substantial reduction of feeding behavior. This contrasts with the normal consumption of a fat meal, which produces little change in subsequent food intake. To determine whether procedural differences account for this discrepancy, we examined the satiating effect of ingested fat on food intake of rats maintained under feeding conditions similar to those employed in studies involving gastrointestinal delivery of fat (i.e., food deprivation, liquid diet). Ingestion of approximately 1.5 ml corn oil had no effect on subsequent liquid diet intake until 90 min after oil ingestion. When rats ingested oil 4 h before access to the liquid diet, to allow time for additional gastrointestinal clearance, liquid diet intake was reduced by 13% in the first 30 min of access. These findings indicate that ingested fat decreases short-term intake slightly, but only if time is allowed for postabsorptive delivery. The results question the physiological significance of the marked suppression of food intake observed in response to administration of fat directly into the gastrointestinal tract.

2,5-anhydro-D-mannitol: a fructose analogue that increases food intake in rats

1988 ◽  
Vol 254 (1) ◽  
pp. R150-R153 ◽  
Author(s):  
M. G. Tordoff ◽  
R. Rafka ◽  
M. J. DiNovi ◽  
M. I. Friedman
Keyword(s):  
Fatty Acids ◽  
Food Intake ◽  
Free Fatty Acids ◽  
Plasma Glucose ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Substrate Analogues ◽  
Increase Food Intake ◽  
Related Increase

We examined the effects on food intake and plasma fuels of 2,5-anhydro-D-mannitol (2,5-AM; 2-deoxy-D-fructose), a fructose analogue that inhibits hepatocyte gluconeogenesis and glycogenolysis in vitro. 2,5-AM (50-800 mg/kg po) given to rats during the diurnal fast produced a dose-related increase in food intake during the 2 h after administration. A 200-mg/kg dose of 2,5-AM decreased plasma glucose, increased plasma ketone bodies, free fatty acids, and glycerol, and had no effect on triglycerides. Normal and diabetic rats given 2,5-AM (200 mg/kg ip) increased food intake to the same extent. These results suggest that, unlike other substrate analogues that increase food intake, 2,5-AM increases feeding by creating a metabolic state that resembles fasting.

Influence of exogenous fatty acids and ketone bodies on rates of lipolysis in isolated ventricular myocytes from normal and diabetic rats

1990 ◽  
Vol 68 (9) ◽  
pp. 1177-1182 ◽  
Author(s):  
Terje S. Larsen ◽  
David L. Severson
Keyword(s):  
Fatty Acids ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Combined Effect ◽  
Diabetic Myocardium ◽  
Streptozotocin Diabetic Rats ◽  
Isolated Ventricular Myocytes ◽  
Stimulation Of

The effect of oleate (0.3 and 1.2 mM) and the combined effect of β-hydroxybutyrate (4 and 8 mM) and acetoacetate (1 and 2 mM) on rates of lipolysis (glycerol output) was determined with calcium-tolerant myocytes isolated from the hearts of normal rats and hearts from acutely (2–3 days; 100 mg/kg streptozotocin) diabetic rats. In addition, the effect of these exogenous substrates on rates of lipolysis was investigated in triacylglycerol (TG) loaded myocytes prepared from normal hearts by inclusion of oleate in the isolation solutions. Diabetic and TG-loaded myocytes had higher lipolytic rates than normal myocytes. In control myocytes, oleate (1.2 mM) did not affect basal lipolysis, but it reduced isoproterenol-stimulated lipolysis by 30%. In diabetic and TG-loaded myocytes, the addition of 1.2 mM oleate inhibited basal rates of lipolysis by 41 and 40%, respectively, and isoproterenol-stimulated rates of lipolysis by 43 and 53%, respectively. However, lipolytic rates measured in the presence of 1.2 mM oleate with diabetic and TG-loaded myocytes were still higher than lipolysis in normal myocytes incubated in the absence of oleate. Ketone bodies increased both basal and isoproterenol-stimulated lipolysis in normal myocytes. In diabetic myocytes, ketone bodies produced a modest stimulation of basal lipolysis but had no effect on isoproterenol-stimulated rates of lipolysis. These data indicate that mobilization of endogenous TG may play an important role in supplying energy to the heart in the diabetic state. Moreover, accumulation of endogenous TG in diabetic myocardium can only partly be explained by inhibition of lipolysis by exogenous substrates.Key words: lipolysis, cardiac myocytes, diabetes.

scholarly journals BZ043, a novel long-acting amylin analog, reduces gastric emptying, food intake, glycemia and insulin requirement in streptozotocin-induced diabetic rats

Peptides ◽  
2019 ◽  
Vol 114 ◽  
pp. 44-49 ◽  
Author(s):  
Caio Victor M.F. Nascimento ◽  
Celimar Sinezia ◽  
Thayna Sisnande ◽  
Luís Maurício T.R. Lima ◽  
Paulo G.S. Lacativa
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Insulin Requirement ◽  
Diabetic Rats ◽  
Long Acting

Dietary fat, hypothalamic glutamate decarboxylase, and food intake of streptozotocin-diabetic rats

1991 ◽  
Vol 261 (6) ◽  
pp. R1554-R1559
Author(s):  
J. L. Beverly ◽  
M. H. Oster ◽  
T. W. Castonguay ◽  
J. S. Stern
Keyword(s):  
Food Intake ◽  
High Fat Diet ◽  
Glutamate Decarboxylase ◽  
Diabetic Rats ◽  
Ventromedial Nucleus ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Streptozotocin Diabetic Rats ◽  
Gad Activity

The association among changes in glucose status, glutamate decarboxylase (GAD) activity, and food intake was evaluated in several hypothalamic areas of streptozotocin-diabetic rats fed a low- (12% of calories as fat) or high-fat diet (59% of calories as fat). Control rats consumed approximately 90 kcal/24 h of either diet, whereas diabetic rats consumed approximately 150 kcal/24 h of the low-fat diet and approximately 100 kcal/24 h of the high-fat diet. At the end of the study, diabetic rats fed the high-fat diet weighed more and had higher retroperitoneal fat depot weights (P less than 0.05) than diabetic rats fed the low-fat diet. In diabetic rats, GAD activity was 15-20% higher in the ventromedial nucleus (P less than 0.01) but similar to controls in the lateral hypothalamus, paraventricular nucleus, and area postrema. Diet did not affect GAD activity in the brain areas studied. The increase in ventromedial nucleus GAD activity was not associated with the level of food intake and was the likely result of altered glucose homeostasis in diabetic rats.

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