Biomedical subjects

M G Tordoff

Publications and source records attributed to M G Tordoff.

At least 19 recordsLinked to original sources

PubMed1992

Experience with a macronutrient source influences subsequent macronutrient selection.

We examined the influence of experience with a macronutrient on subsequent macronutrient selection. For 4 days, rats ate chow, or chow and a single macronutrient source. They then had simultaneous access to protein, carbohydrate (CHO) and fat sources, according to a standard macronutrient self-selection paradigm. When selecting among the macronutrient sources, rats pre-exposed to CHO ate more CHO, and those pre-exposed to fat ate more fat, relative to the other groups. Rats pre-exposed to protein ate more protein than did those pre-exposed to CHO or fat but not more than those that received no macronutrient pre-exposure. These selection patterns persisted for at least 12 days, when the test was ended because of the low protein intakes and poor growth of the rats pre-exposed to the CHO and fat sources. After 34 days of recovery with only chow to eat, the rats were again allowed to choose among the three macronutrients, and their patterns of selection were essentially unchanged. Similar results were found in a second experiment in which a 5-day interval was interposed between macronutrient pre-exposure and macronutrient selection. These findings show that experience with the macronutrients typically used in self-selection experiments can have a large, long-lasting, and sometimes detrimental effect on subsequent food selection by rats. Prior experience can be a more powerful influence than nutritional wisdom in determining the rat's food choice.

Animals↗

PubMed1992

Salt intake of rats fed diets deficient in calcium, iron, magnesium, phosphorus, potassium, or all minerals.

Groups of nine to ten male rats fed diets deficient in calcium, iron, magnesium, phosphorus, potassium, or all minerals (i.e. no mineral mix) were given 0.3 M NaCl and water to drink. Over the first 30 days of dietary treatment, 0.3 M NaCl intake was progressively increased by deprivation of calcium or iron, unaltered by deprivation of phosphorus, and increased and then decreased by deprivation of magnesium, potassium, or all minerals. The changes in NaCl intake of rats deprived of potassium or all minerals were matched by corresponding changes in water intake. Water intakes of the other groups were unaltered. Thus, NaCl preference was increased by deprivation of calcium or iron, unaltered by deprivation of phosphorus, potassium, or all minerals, and decreased by deprivation of magnesium. To determine whether these changes were specific to the salty modality, animals maintained for 32 days on the diets deficient in calcium, iron, magnesium, and phosphorus received 24-h two-bottle tests with water vs. 2.5 mM saccharin, 2.5 mM citric acid, 0.368 mM sucrose octa-acetate, or 0.3 M NaCl. Relative to controls, rats deprived of calcium drank less 2.5 mM saccharin, those deprived of magnesium drank less 0.3 M NaCl, and those deprived of calcium or iron drank more 0.3 mM NaCl. These results show that different mineral deficiencies have different effects on NaCl intake. They argue against the hypothesis that animals deprived of any mineral develop a chronic appetite for salt.

Animals↗

PubMed1992

Influence of dietary calcium on sodium and calcium intake of spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHRs) fed nutritionally complete diets voluntarily ingest more calcium and more NaCl solution than do their normotensive Wistar-Kyoto (WKY) controls. SHRs also have several anomalies in calcium metabolism. Given that calcium availability modulates NaCl intake of other rat strains, we examined whether sodium and calcium intake of the SHR was unusually responsive to manipulations of dietary calcium. In three experiments, groups of SHRs and WKYs ate diets differing in calcium content (0-1,000 mmol/kg) and drank solutions of sodium (50 and 300 mM NaCl or 50 mM sodium lactate) and/or calcium (50 and 110 mM calcium lactate or 50 mM CaCl2). Relative to WKYs, SHRs fed calcium-deficient diet (0 mmol Ca2+/kg) drank the same amount or less calcium solution, drank more NaCl, and increased NaCl intake more rapidly when the diet was first introduced. SHRs fed diets sufficient for normal growth (50-1,000 mmol Ca2+/kg) drank consistently more calcium and sodium solution than did WKYs. However, NaCl intake of SHRs was decreased by high-calcium diets, whereas NaCl intake of WKYs was not. Taken together, these results suggest that a mechanism dependent on the availability of calcium is at least partially responsible for the high salt intake of the SHR.

Analysis of Variance↗

PubMed1991

Calcium deprivation increases NaCl intake of Fischer-344 rats.

Fischer-344 rats fed Ca2(+)-deficient diet for 63 days increased intake of 0.3 M NaCl solution from control levels of approximately 8 ml/day to greater than 60 ml/day. During the same period, rats fed Na(+)-deficient diet drank approximately 11 ml/day. These results indicate that Fischer-344 rats, which generally spurn NaCl, drink large amounts of it when Ca2+ deprived.

Animals↗

PubMed1991

Sham-feeding sucrose or corn oil stimulates food intake in rats.

In separate experiments, rats with open gastric cannulas were sham-fed either 32% sucrose solution or 15% corn oil emulsion. The rats' cannulas were then closed, and food intake was measured for 2 h. Food intake was greater after sham-feeding either fluid than after tests when no fluid was available. These results suggest that the oral stimulation produced by ingestion of sweet or oily fluids can stimulate appetite in the rat.

Administration, Oral↗

PubMed1991

2,5-anhydro-D-mannitol acts in liver to initiate feeding.

We determined the site at which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) acts to increase food intake in rats. Rats began eating sooner and ate more food during hepatic portal than during jugular infusions of 2,5-AM (50, 100, or 150 mg/h). After rats were intubated with 2,5-[14C]AM (1.15 microCi in 200 mg/kg), significant quantities of radioactivity were found in liver but not in brain. Hepatic vagotomy prevented the eating response to 200 mg/kg 2,5-AM without altering the effect of the analogue on plasma fuels. These results indicate that low doses of 2,5-AM act in the liver to increase food intake and suggest that the signal for feeding generated in the liver is transmitted to the brain through the hepatic vagus nerve. Taken together, this work provides the strongest evidence to date that a signal initiating feeding behavior originates in the liver.

Animals↗

PubMed1991

Physiological consequences of NaCl ingestion by Na(+)-depleted rats.

We investigated the temporal relationships between NaCl intake, gastrointestinal Na+ content, and plasma concentrations of Na+, aldosterone, and plasma renin activity (angiotensin). Rats depleted of approximately 2.2 mmol Na+ by combined dietary Na+ restriction and furosemide injection (10 mg sc) drank a preload of 1, 2, or 3 mmol 0.5 M NaCl. Intake of a test 0.5 M NaCl solution given 15, 30, 60, or 120 min later was reduced by approximately 50% of the preload content, irrespective of the interval between preload and test. At 15 min after starting to drink, 61-71% of ingested Na+ remained in the stomach, 15-18% in the small intestine, approximately 5% was calculated to be in extracellular fluid, and less than 1% was excreted. Rates of gastric and gastrointestinal clearance of Na+ were related to the quantity of NaCl ingested. Whereas gastric emptying was initially very rapid (30-61 mumol/min) and decreased with time, gastrointestinal clearance was constant (16-39 mumol/min). Drinking 3 mmol NaCl reliably reduced plasma aldosterone concentrations within 15 min and renin activity within 30 min. Drinking 1 or 2 mmol NaCl reliably reduced levels of these hormones within 30-60 min. The results describe for the first time the distribution of Na+ after Na(+)-depleted rats drink NaCl. They suggest that the rat determines the quantity of Na+ it requires within the first 15 min of ingestion and thus does not depend on signals generated by the prolonged influence of Na+ in the gastrointestinal tract or the fall in plasma concentrations of aldosterone and angiotensin.

Administration, Oral↗

PubMed1991

Enhanced acceptance and metabolism of fats by rats fed a high-fat diet.

Rats fed a high-fat diet show greater acceptance of and preference for pure fats than do rats fed a high-carbohydrate diet. We tested the hypothesis that this differential intake of fat was due to diet-induced modifications of lipid absorption and oxidation. After an intragastric load of corn oil, rats adapted to a high-fat diet had greater increases in plasma triglyceride and ketone levels and a lower percentage of fecal fat than did rats adapted to an isocaloric high-carbohydrate diet. High-fat-fed rats given corn oil containing [14C]palmitic acid expired 14CO2 more rapidly and to a greater extent than did rats maintained on a high-carbohydrate diet. These results show that the greater acceptance of fat by rats fed a high-fat diet is associated with an increased capacity to absorb and oxidize fat.

Animals↗

PubMed1990

Sham-feeding of corn oil by rats: sensory and postingestive factors.

Previous research indicates that rats fed a high-fat (HF) diet increase their intake and preference for oil compared with rats fed a high-carbohydrate (HC) diet. To assess whether this increased intake was due to the sensory or postingestive properties of oil, rats were adapted to either the HF or HC diet and then allowed to sham-feed pure corn oil daily for 30 min. During the first 4 trials, rats fed the HF diet sham-fed more oil than did rats fed the HC diet; however, this difference diminished with repeated testing and was absent after 8 trials. In both diet groups, 4-5 calories (approximately 25%) of sham-fed oil could not be recovered and may have escaped to the intestine. These results suggest that, compared with rats fed a HC diet, rats fed a HF diet are initially attracted to the sensory properties of oil, but that the differential oil intakes of rats fed the HF or HC diet are maintained by postingestive, rather than sensory factors.

Animals↗

PubMed1990

Oral stimulation with aspartame increases hunger.

We evaluated whether "sweetness" increases hunger. Groups of 10 male and 10 female subjects chewed a gum base containing one of four concentrations of aspartame (0.05%, 0.3%, 0.5%, or 1.0%) for 15 min. Relative to groups given nothing or unsweetened gum base to chew, groups given the sweetened gum bases increased hunger ratings, but not in a manner monotonically related to aspartame concentration. The most effective aspartame concentration to increase hunger was 0.3% for females and 0.5% for males. The highest aspartame concentrations had a time-dependent, biphasic effect on appetite, producing a transient decrease followed by a sustained increase in hunger ratings. Thus, the concentration of the sweetener, the sex of the subject and the time after chewing, were all important determinants of whether "sweetness" increased hunger.

Adult↗

PubMed1990

Flavor preferences and fructose: evidence that the liver detects the unconditioned stimulus for calorie-based learning.

Previous work suggests that fuel oxidation in the liver provides an unconditioned stimulus for "calorie-based" flavor preference learning. To investigate this possibility in more detail, we manipulated liver metabolism by taking advantage of the greater specificity to the liver of fructose than glucose. Intact rats preferred flavored food ingested with a drink of 35% fructose solution to flavored food eaten with either no sweet drink (Experiment 1) or an equicaloric drink of glucose (Experiment 2). The effect on food preference did not depend on the taste of the sugar solutions: when given a choice between glucose and fructose solutions, the rats drank the same volume of each. Moreover, a preference for fructose-paired flavored food was obtained when fructose and glucose solutions were given by gavage (Experiment 3). Unlike intact rats, rats with hepatic vagotomy preferred equally flavored food paired with fructose solution and flavored food paired with no sugar solution (Experiment 1). They also avoided flavored food paired with gavage of fructose slightly, relative to flavored food paired with gavage of glucose (Experiment 3). These results suggest that the unconditioned stimulus for calorie-based conditioning is transduced in the liver, and that an intact hepatic vagus nerve is required for conditioning to occur.

Animals↗

PubMed1990

Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight.

To examine whether artificial sweeteners aid in the control of long-term food intake and body weight, we gave free-living, normal-weight subjects 1150 g soda sweetened with aspartame (APM) or high-fructose corn syrup (HFCS) per day. Relative to when no soda was given, drinking APM-sweetened soda for 3 wk significantly reduced calorie intake of both females (n = 9) and males (n = 21) and decreased the body weight of males but not of females. However, drinking HFCS-sweetened soda for 3 wk significantly increased the calorie intake and body weight of both sexes. Ingesting either type of soda reduced intake of sugar from the diet without affecting intake of other nutrients. Drinking large volumes of APM-sweetened soda, in contrast to drinking HFCS-sweetened soda, reduces sugar intake and thus may facilitate the control of calorie intake and body weight.

Adult↗

PubMed1990

Fuel partitioning and food intake: role for mitochondrial fatty acid transport.

Administration of methyl palmoxirate (MP; 10 mg/kg po), an inhibitor of carnitine palmitoyltransferase I (CPT I), increased the food intake of rats maintained on a diet high in triglycerides comprised of long-chain fatty acids, which require CPT I for mitochondrial uptake and oxidation. MP did not affect food intake in rats fed a comparable diet high in medium-chain fatty acids, which do not require CPT I for mitochondrial uptake and oxidation. The feeding response to MP was reduced more effectively by an intragastric preload of medium-chain triglyceride (MCT) oil than a preload of a long-chain triglyceride (LCT) oil. Food intake of MCT- and LCT-fed rats differed under control conditions (no MP), and this appeared to reflect differences in the diurnal distribution of feeding. Measurement of plasma ketone body concentrations indicated that the dietary manipulations and MP had their intended metabolic effects. The results strongly suggest that mitochondrial transport of fatty acids plays a role in the control of food intake. CPT I participates in that control by regulating the partitioning of long-chain fatty acids between pathways of storage and intramitochondrial oxidation.

Adipose Tissue↗

PubMed1990

Calcium deprivation increases salt intake.

Relative to rats fed chow or semisynthetic control diet, rats fed Ca2(+)-deficient diet increased daily "spontaneous" intake of 0.3 M NaCl solution by as much as eightfold. Intake of 0.3 M NaCl increased in monotonic relationship to the severity of Ca2+ deficiency, which was manipulated by both duration of depletion (0-32 days) and dietary Ca2+ content (0-50 mmol/kg Ca2+). The increased intake was specific to either Na+ or saltiness; relative to controls, Ca2(+)-deprived rats drank more of a wide range of NaCl solutions (0.05-0.50 M) but the same volume of 0.37 mM sucrose octaacetate (bitter), slightly more 2.5 mM citrate (sour), and significantly less 2.5 mM saccharin (sweet). Although urine volume of Ca2(+)-deprived rats was increased, total Na+ excretion was slightly decreased. Adrenal weights, hematocrit, and plasma concentrations of Na+, aldosterone, and angiotensin I were all normal. These results reveal that Ca2+ deficiency increases NaCl intake and thus challenge the notion that salt appetite is a specific response to perturbed Na+ homeostasis.

Animal Feed↗

PubMed1989

Dietary hyperphagia and obesity: what causes them?

Diets that cause animals to overeat and become obese have been used in many investigations of obesity. Most of this research, however, has concentrated on the consequences rather than the causes of overeating. Furthermore, in most studies, several nutritional variables were manipulated simultaneously, making cause and effect relationship impossible to disentangle. Consequently, progress has been slow. Diets could alter energy intake by virtue of their effects on oral-sensory, gastrointestinal or postabsorptive effects. Palatability is the most popular oralsensory hypothesis but the empirical basis for this hypothesis is particularly weak. A substantial body of evidence is consistent with the possibility that the osmotic effects of diets in the gastrointestinal tract and metabolic postabsorptive factors may play a major role in dietary hyperphagia and obesity. Suggestions for future research directions are offered.

Animals↗

PubMed1989

Drinking saccharin increases food intake and preference--I. Comparison with other drinks.

To examine the orosensory and postingestive effects of saccharin solution on food intake and food preference, freely feeding rats were given flavored food to eat and a solution to drink for 2 h on eight to ten occasions. Relative to trials with a different flavored food and only water to drink, food intake was increased by drinking 0.2% saccharin or 0.45% NaCl, unaffected by drinking 1% almond extract, and decreased by drinking 10% glucose. Food preference, which was assessed in a choice test with simultaneous access to the two flavored foods, was increased by drinking 0.2% saccharin or 10% glucose and unaffected by drinking 1% almond extract or 0.45% NaCl. These results are consistent with the possibility that a combination of the oral and hydrational properties of saccharin solution increase food intake. Saccharin's sweet taste may be responsible for its effects on food preference.

Animals↗

PubMed1989

Drinking saccharin increases food intake and preference--II. Hydrational factors.

Rats that drink saccharin solution increase their short-term food intake and develop a preference for flavored food eaten when saccharin is ingested. In this paper, we examined whether these changes in feeding behavior were due to overhydration resulting from drinking hyposmotic saccharin solution. Consistent with this possibility, the short-term food intake of rats was increased by drinking hyposmotic 0.2% saccharin dissolved in water, unaffected by drinking isosmotic 0.9% NaCl, and decreased by drinking 0.2% saccharin dissolved in 0.9% NaCl. In addition, rats showed a sustained increase in saccharin-induced food intake after antidiuretic hormone treatment, which was designed to exacerbate their positive water balance. Less consistent with a hydrational explanation of saccharin-induced feeding was the finding that rats drinking only 2ml 0.2% saccharin solution increased food intake. Also, gastric intubation of similar volumes of water produced a small, transient increase in feeding behavior, which was apparent after the first intubation only and could not be preserved by adding water-contingent flavors to the food. Taken together, these results suggest that the hydrational effects of drinking hyposmotic saccharin solution contribute to, but cannot account for, the increase in food intake. Hydration had no observable influence on the acquisition of flavored food preference.

Animals↗

PubMed1989

Drinking saccharin increases food intake and preference--III. Sensory and associative factors.

Rats that drink saccharin solution increase their short-term food intake and develop a preference for flavored food eaten when saccharin is ingested. Here we describe experiments that examined whether these changes in feeding behavior were due to learning and/or the reinforcing sensory properties of saccharin solution. It was found that learning was unnecessary for the feeding response, as rats that drank saccharin increased food intake whether or not their food contained saccharin-contingent flavor cues. However, learning helped support and maintain the response, as rats repeatedly given flavored food together with saccharin to drink later increased intake when given the flavored food without saccharin (i.e. in extinction). The rewarding or hedonic effects of the immediate orosensory properties of saccharin were not responsible for its effects on feeding, as drinking saccharin before but not after eating flavored food increased food intake and food preference. Furthermore, hungry rats developed an aversion to flavored food paired with saccharin ingestion when the quantity of food was limited. This implies that the flavored food preference produced by drinking saccharin involves an association between sensory aspects of the food and the metabolic consequences of food ingestion, which interact with a postingestive action of drinking saccharin that is related to the rat's metabolic state.

Animals↗