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Biomedical subjects

M I Friedman

Publications and source records attributed to M I Friedman.

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↗
PubMed1991

Altered acceptability of and preference for sugar solutions by diabetic rats is normalized by high-fat diet.

Two experiments examined the ingestive responses of streptozotocin-diabetic rats fed low-fat or high-fat diets to glucose, fructose, sucrose and maltose solutions in brief (30 min) intake tests. In Experiment 1, one-bottle acceptability tests were used whereas two-bottle preference tests were used in Experiment 2. Three main findings resulted from these studies. Firstly, diabetic rats fed the low-fat diet displayed a reduced acceptance of and preference for all concentrated sugar solutions. Secondly, glucose consumption patterns of diabetic rats fed the low-fat diet were distinctly different from their responses to the other sugars. Thirdly feeding high-fat diets, either high or low in carbohydrate, normalized the responses of diabetic rats to the sugar solutions. The results suggest that feeding high-fat diets to diabetic rats normalizes their responses to sugar solutions because of reductions in hunger and thirst associated with the provision of a utilizable source of calories and an improvement in body fluid balance.

Analysis of Variance↗
PubMed1991

Role of the transitional mucosa of the colon in differentiating primary adenocarcinoma from carcinomas metastatic to the colon. An immunohistochemical study.

Differentiation between primary colonic adenocarcinoma arising in flat mucosa and carcinoma metastatic to the colon is often difficult. Examination of the mucosa adjacent to the tumor, the so-called transitional mucosa (TM), may be helpful. The morphologic, ultrastructural, and histochemical characteristics of the TM have been reported previously in detail. In this study the morphologic and immunohistochemical characteristics of the TM have been compared in 18 cases of primary colonic adenocarcinoma and 13 cases of metastasis to the colon. Five immunophenotypic markers were used: carcinoembryonic antigen (CEA), Lewis (x) and (y) blood group antigens, ras oncogene p21, and tumor-associated glycoprotein (TAG-72). Neoplastic transformation of colonic epithelium is associated with altered expression of these antigens. The morphologic and immunohistochemical profile of the TM was similar in both primary colonic adenocarcinomas and metastases to the colon. In some cases the TM adjacent to colonic metastases stained with one or more antibodies while the metastatic tumor was negative. Therefore, in cases where differentiation between primary colonic adenocarcinoma arising in flat mucosa and metastasis is difficult, the use of these reagents, particularly CEA, TAG-72, or ras oncogene p21, may be helpful. The similar immunohistochemical staining pattern of the TM in both primary and metastatic colon lesions supports a reactive, non-neoplastic origin of the TM. Furthermore, expression of these antigens is not limited to neoplastic epithelial cells.

Adenocarcinoma↗
PubMed1991

Insulin-induced anestrus in Syrian hamsters.

In Syrian hamsters, reproduction is sensitive to the availability of metabolic fuels. Estrous cycles can be interrupted by brief periods of food deprivation, by pharmacological inhibition of glycolysis and fatty acid oxidation, or by increasing energy demands for thermoregulation. We predicted that manipulations that divert an excessive portion of the metabolic fuel supply into storage also should inhibit reproduction. Redirection of metabolic fuels from oxidation to storage was accomplished by treatment with protamine zinc insulin suspension (PZI). Syrian hamsters treated with PZI and fed ad libitum increased their food intake by approximately equal to 40% and body fat stores, but there was no effect on estrous cycles. When PZI-treated hamsters were limited to approximately equal to 110% of their preinjection food intake, they still fattened, and there was a significant inhibition of estrous cyclicity. Thus, in the absence of overeating, PZI-enhanced energy storage may lead to a shortage of oxidizable metabolic fuels with the result that reproduction is inhibited in favor of processes essential for survival (e.g., cellular maintenance, thermoregulation). It is unlikely that insulin-induced anestrus is due to actions of PZI unrelated to metabolic fuel partitioning, because the hormone had no effects on estrous cyclicity in ad libitum-fed hamsters. These findings are inconsistent with the hypothesis that nutritional infertility is due to the failure to maintain a minimum body fat content and raise the possibility that the infertility associated with some types of obesity could be due in part to a disorder of macronutrient partitioning.

Anestrus↗
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

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

Dietary hyperphagia in rats: role of fat, carbohydrate, and energy content.

Dietary energy, fat and carbohydrate content were varied to determine the nutritional factors responsible for hyperphagia induced by feeding rats high-fat diets. In the first experiment, rats were fed isoenergetic high-fat or high-carbohydrate diets for 2 weeks. Weight gain and energy intake were lower in rats given the high-fat diet. When some of the rats were switched to a diet that was high in fat, carbohydrate and energy, gram food intake was initially unchanged, resulting in a substantial increase in energy intake and weight gain. Energy intake gradually declined over the 4 weeks following the switch to the high-energy diet. In the second experiment, rats were fed high-fat diets that were either high or low in carbohydrate content and either high or low in energy content (kcal/g). Rats fed a high-fat diet that was high in energy and carbohydrate ate the most energy and gained the most body weight and carcass fat. In the third experiment, rats were fed high-carbohydrate diets varying in fat and cellulose content. Energy intake and body weight gain varied directly as a function of caloric density regardless of the fat or cellulose content of the diets. It is concluded that hyperphagia induced by feeding high-fat diets is not due to the high dietary fat content alone. Rather, high levels of fat, carbohydrate, and energy interact to produce overeating and obesity in rats fed high-fat diets.

Animals↗
PubMed1990

Diet composition alters the acceptance of fat by rats.

The acceptance of dietary fat by rats is influenced by changes in fat digestion and metabolism. In these experiments, rats were fed diets that differed in fat, carbohydrate and fiber content, and the acceptance of fat was measured. Rats fed a high fat (HF) diet ate more corn oil in 30-min or 6-h tests than did rats fed an isocaloric high carbohydrate (HC) diet. This effect was seen after the diets were switched and rats retested. Differences in dietary fiber between the isocaloric HF and HC diets did not account for this effect because rats fed HF diets, either high or low in fiber content, drank more oil than rats fed the HC diet. Rats fed the HF diet with added carbohydrate drank less oil than rats fed the HF diet, and the same amount of oil as rats fed the HC diet. Compared with rats fed the HC diet, rats fed the HF diet drank more oil in a two-bottle preference test with sucrose or when mixed with sucrose in a single-bottle test. Rats offered a variety of fats, sugars or other test foods, ate more nutritive liquid fats and some solid fats, but did not eat more sugar or other items if they were fed the HF diet rather than the HC diet. These studies taken together strongly suggest that rats fed a high fat diet show a greater acceptance of fat compared with rats fed a high carbohydrate diet.

Animals↗
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

Body fat and the metabolic control of food intake.

The role of body fat in the control of food intake is considered from the point of view that the oxidation of metabolic fuels generates a signal that governs feeding behavior. According to this perspective, the storage and mobilization of fat affect food intake indirectly by altering fuel oxidation. Hyperphagia during the development of obesity is thus treated as an appropriate response to a primary metabolic defect that causes fuels to be stored rather than oxidized. Evidence is presented that changes in insulin level and the activity of carnitine palmitoyltransferase I modulate feeding by altering the partitioning of fatty acids. The possibility that dietary interactions, acting through these mechanisms, may cause overeating of high-fat diets is discussed. It is proposed that the signal for feeding originates in the liver when both fatty acids and glucose are unavailable for oxidation.

Adipose Tissue↗
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

Diabetes and a high-fat/low-carbohydrate diet enhance the acceptability of oil emulsions to rats.

Acceptability of corn oil and coconut oil emulsions was examined in streptozotocin-diabetic (55 mg/kg, IP) and normal rats fed either a high-fat/low-carbohydrate (HF/LC) or low-fat/high-carbohydrate (LF/HC) diet. Intake of five concentrations of the emulsions (2.5, 5, 10, 20 and 40%) was measured in 30-min, one bottle intake tests. Diabetic rats consumed more of the oil emulsions than did normal rats. Emulsion intake by diabetic rats increased, then decreased across concentrations, whereas emulsion intake by normal rats showed little change across concentrations. No differences in the intake of corn and coconut oil emulsions were observed. Total oil consumption was higher in diabetic than in normal rats at the three highest emulsion concentrations. Total oil consumption was also higher in rats fed the HF/LC diet as compared to those fed the LF/HC diet. These findings suggest that the presence of diabetes or feeding a HF/LC diet can enhance oil emulsion intake of rats in short-term tests.

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↗
PubMed1989

Drinking saccharin increases food intake and preference--IV. Cephalic phase and metabolic 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 effects are mediated by cephalic-phase metabolic reflexes. The results show that the cephalic-phase insulin response could be dissociated from food intake in three ways. (1) Drinking saccharin increased the food intake and food preference of rats with sham surgery (SHM) or celiac vagotomy (CV), but not hepatic vagotomy (HV); it produced a short-lived increase in plasma insulin levels in all three groups, but the insulin response of both the CV and HV group was attenuated relative to the SHM group. (2) Rats increased food intake even when a 90 min interval was imposed between drinking saccharin and eating food, although insulin and glucose levels returned to normal within 30 min of drinking saccharin. (3) Streptozotocin-induced diabetes did not affect the increased feeding response to saccharin. The failure of rats given hepatic vagotomy to increase food intake and food preference when drinking saccharin suggests that a hepatic mechanism is involved. We propose that drinking saccharin increases food intake by temporarily altering the disposition of metabolic fuels towards storage and away from oxidation. Flavored food eaten after drinking saccharin becomes preferred because it provides fuel to counteract this reduction in oxidation.

Animals↗