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PubMed2006

The fatty acid pattern of dietary fat influences the oral bioavailability of the flavonol quercetin in pigs.

We have shown recently that dietary fat content influences the bioavailability of the flavonol quercetin. In the present study, the influence of the fatty acid pattern of dietary fats on the oral bioavailability of quercetin was investigated. Quercetin (30 micromol/kg body weight) was administered to growing pigs (n 6) in test meals consisting either of 200 g of a standard pig diet (2% crude fat) or of the same diet supplemented with 15 g fat/100 g diet using either medium-chain (MCT) or long-chain fatty acid triacylglycerols (LCT). Blood samples were drawn repeatedly over a period of 24 h and analysed by HPLC. In addition, the influence of the different diets on gastric emptying was investigated in rats. In pigs, the bioavailability of quercetin was measured by quantifying its plasma metabolites with an intact flavonol structure. Bioavailability was enhanced by 38% (P<0.05) and 12% (P>0.05) after intake with the MCT and LCT diets, respectively, compared to the standard diet. Maximum plasma concentrations of quercetin were reached significantly later with the MCT diet than with the LCT or the standard diet (P<0.05). No differences in dry matter of the gastric content were observed 60 min after intake of the experimental diets in rats. Thus, administration of quercetin together with a diet containing MCT fat enhances the bioavailability of the flavonol. Absorption of quercetin was delayed significantly with this diet. However, this was probably not due to slower gastric emptying of the MCT diet.

Animals↗

PubMed1986

Dietary fat and neoplasia--the role of net energy in enhancement of carcinogenesis: effects of fat and calories on the immune system.

The mechanism by which carcinogenesis is enhanced by dietary fat is not understood. We know that a minimum level of essential fatty acids (EFA) is necessary for mammary tumor development and that this level probably exceeds the normal requirements of rats. Once the minimum level of EFA has been supplied, the calorie contribution of dietary fat may account for its enhancement of carcinogenesis. In this regard, we must recognize that the efficiency with which dietary energy is utilized is known to increase as the fat content of the diet is raised. Hence even when fed isocalorically to low fat diets, high fat diets will provide more net energy. Modulation of host immunity has been proposed as a mechanism of action of both fat and calorie intake on neoplasia. We review the literature examining the effects of fat and calories on the cell-mediated immune system, that arm of the immune system most directly responsible for the killing of neoplastic cells.

Dietary Fats↗

PubMed1998

Regulation of apolipoprotein B-containing lipoproteins by vitamin C level and dietary fat saturation in guinea pigs.

Effects of suboptimal and adequate vitamin C, with varying dietary fat saturation, on hepatic cholesterol and plasma lipoprotein concentrations and metabolism were studied in guinea pigs fed 15% (wt/wt) fat/0.04% cholesterol diets. Fat mixtures were either 49% saturated (SFA) (24% lauric acid) or 53% polyunsaturated fatty acid (PUFA) linoleic acid with vitamin C at 50 (suboptimal) or 500 (adequate) mg/kg diet. Guinea pigs fed suboptimal vitamin C had 15% lower hepatic active 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and 25% lower low-density lipoprotein (LDL; apolipoprotein [apo] B/E) receptor number, 20% higher acyl-CoA:cholesterol acyltransferase (ACAT) activity, 28% higher triacylglycerol (TAG) and cholesteryl ester concentrations, and increased very-low-density lipopoprotein (VLDL) apo B secretion rates in comparison to animals fed adequate vitamin C. Intake of suboptimal vitamin C lowered plasma high-density lipoprotein (HDL) cholesterol concentrations by 45% and increased plasma TAG, total and VLDL/LDL cholesterol, and cholesteryl ester transfer protein (CETP) activity by 40%, 50%, and 30%, respectively. The hyperlipidemic effects of suboptimal vitamin C were more pronounced with intake of the SFA diet. These data demonstrate that low vitamin C intake results in a pattern of changes in whole-body cholesterol and lipoprotein metabolism that are related to increased risk of cardiovascular disease (CVD).

Animals↗

PubMed1998

Broiler breeder age and dietary fat influence the yolk fatty acid profiles of fresh eggs and newly hatched chicks.

The purpose of the present study was to investigate the combined effects of breeder age (36-, 51-, or 64-wk) and different dietary fat sources (3% added corn oil, poultry fat, or lard) on lipids in fresh egg yolks and yolks of newly hatched chicks. Isocaloric breeder diets were altered by the inclusion of different types of dietary fat such that the poultry fat and lard diets had the highest levels of saturated fatty acids when compared to the corn oil diet. Fresh egg yolks obtained from 36-wk-old breeders exhibited higher levels of palmitoleic acid when compared to the levels observed in fresh egg yolks of 51- or 64-wk-old breeders. Furthermore, these levels decreased significantly by 21 d of incubation only in eggs from 36-wk-old hens. At 36 wk of breeder age, the levels of oleic and arachidonic acid were higher in yolks from hatched chicks than in previous fresh egg values, regardless of type of added dietary fat; whereas the level of linoleic acid was higher only in yolks from hatched chicks compared to those of fresh eggs from 36-wk-old hens fed 3% added corn oil. These data suggest that breeder age influences the utilization of yolk lipid by developing embryos, and that the type of fat provided in the diet may have an additional influence.

Adipose Tissue↗

PubMed1986

Effect of colon tumor development and dietary fat on the immune system of rats treated with DMH.

We examined the effect of dietary fat and colon tumorigenesis on the morphology and function of the rat mesenteric lymph node (MLN) and spleen at two stages of tumor development. Male Sprague-Dawley rats were fed semipurified diets of varying fat content (5% mixed fat, 24% beef fat, 24% corn oil, or 24% Crisco) and treated for five weeks with either the colon carcinogen 1,2-dimethylhydrazine (DMH) or the vehicle (saline). Animals consuming high-fat diets had an increased incidence of splenic follicular and germinal center hyperplasia. Carcinogen treatment had no significant effect on the histological morphology of the spleen. MLN morphology was not dramatically affected by either diet or DMH treatment. At this time period, the splenic lymphocyte transformation response induced by concanavalin A (Con A), phytohemagglutinin, or pokeweed mitogen was significantly depressed in the group fed 24% corn oil (vehicle-treated) and in the DMH-treated groups fed 5% fat compared with the vehicle-treated group fed 5% fat. In contrast, the MLN transformation response was elevated in the group fed 24% Crisco. DMH treatment did not significantly influence the MLN response. Four months after carcinogen or vehicle treatment, at the point of colon tumor development, no statistically significant differences were seen in the splenic or MLN blastogenic responses of DMH- or saline-treated animals. Splenic natural killer cell cytotoxic activity was also not significantly affected by dietary fat, carcinogen treatment, or tumor development.

1,2-Dimethylhydrazine↗

PubMed1982

The lipolytic triad: human lingual, breast milk, and pancreatic lipases: physiological implications of their characteristics in digestion of dietary fats.

The characteristics of human lingual, breast milk, and pancreatic lipases as related to the digestion of dietary fats in infants are discussed. The activity and specificity of these enzymes and structure of the dietary fats largely determine the rates of lipolysis, the types of digestion products formed, and the rates of absorption. Also possibly influenced are micelle formation, intestinal health, breast milk jaundice, and the absorption of other nutrients. In premature infants, the action of lingual and breast milk lipase are particularly important in the absorption of dietary fatty acids.

Bile Acids and Salts↗

PubMed1995

Dietary fat alters the distribution of cholesterol between vesicles and micelles in hamster bile.

The type of dietary fat strongly affects the incidence of gallstones in the hamster model of cholesterol cholelithiasis. The present study was designed to determine whether dietary fats could affect gallstone formation by altering the microstructure (vesicular/micellar ratio) of cholesterol in bile. Golden Syrian hamsters from Sasco (Omaha, NE) or Charles River (Wilmington, MA) were fed nutritionally adequate semipurified diets to which were added: (i) 4.0% butterfat without added cholesterol; (ii) 1.2% palmitic acid plus 0.3% cholesterol; or (iii) 4.0% safflower oil plus 0.3% cholesterol. Gallstone incidence and the percentage of cholesterol in vesicles and micelles were determined after two- or six-week feeding periods. Three out of ten Sasco hamsters fed the 1.2% palmitic acid diet for two weeks had cholesterol stones, while none of the eight Charles River animals had stones. In the Sasco hamsters, a significant proportion of the biliary cholesterol was found in void volume vesicles (28.8%) and small vesicles (17.1%); Charles River hamsters had negligible proportions (1.1%) of cholesterol in void volume vesicles and 15.4% in small vesicles. Cholesterol gallstones were most abundant in Sasco hamsters fed 1.2% palmitic acid for six weeks (nine out of ten animals); the mean cholesterol saturation index of the bile was 1.27. A significant proportion of the biliary cholesterol was eluted in the void volume vesicles (21.4%) and in small vesicles (15.0%). Five of the eight identically treated Charles River hamsters had cholesterol stones; the cholesterol saturation index averaged 1.36, and the biliary cholesterol was present in void volume vesicles (31.3%) and small vesicles (14.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Effect of dietary fat composition on rat colon plasma membranes and fecal lipids.

The present study was designed to examine the effect of dietary fat composition on the structure of colon mucosal plasma membranes and fecal lipids. Rats were fed a purified diet containing 14% of either highly saturated fat (beef fat or butterfat) or highly polyunsaturated oil (safflower) in addition to 2% corn oil for 4 wk. Colon mucosal membranes were prepared and examined for lipid composition and protein pattern. Saturated fatty acid feeding resulted in the loss of some protein bands from plasma membranes compared to feeding polyunsaturated fatty acids. Within the saturated fatty acid--rich fats, feeding beef fat caused a greater loss than did feeding butterfat. Dietary fat composition had no effect on membrane content of phospholipid and cholesterol. Saturated fatty acid feeding resulted in an increase in the percentage of 18:1 in plasma membrane lipids compared to feeding safflower oil. The observed changes in the structure of colon mucosal membrane of animals fed the saturated fats were associated with an increase in fecal free fatty acids. There was a 4-fold and 2-fold increase in fecal free fatty acids with feeding the beef fat and butterfat diets, respectively, compared to the safflower oil diet. Alterations in fecal bile acid and free fatty acid composition were also noticed with feeding saturated fatty acids. The results obtained suggest that feeding saturated fatty acids as the main source of fat in the diet could influence the structure of colon mucosa, and this could be mediated through fecal free fatty acids.

Animal Feed↗

PubMed1994

Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) Study.

Associations between atherosclerosis and dietary fat and cholesterol have been demonstrated in numerous animal experiments. The relation between these dietary components and atherosclerosis has not previously been reported in a population-based study among human beings. The associations of dietary fat and cholesterol with carotid artery wall thickness (atherosclerosis) were investigated in a population-based study, the Atherosclerosis Risk in Communities (ARIC) Study, from 1987 to 1989. Participants were 2,095 black women, 5,146 white women, 1,318 black men and 4,589 white men, aged 45-64 years, recruited from four US communities: Jackson, Mississippi; Forsyth County, North Carolina; Washington County, Maryland; and Minneapolis, Minnesota. Habitual diet was assessed with a food frequency questionnaire. Wall thickness was measured with B-mode ultrasound. After adjustment for age and energy intake, animal fat, saturated fat, monounsaturated fat, cholesterol, and Keys' score were positively related to wall thickness, while vegetable fat and polyunsaturated fat were inversely related to wall thickness. These associations persisted after further adjustment for smoking and hypertension and were consistent across the four race and sex groups. Thus, elements of habitual dietary intake were consistently associated with carotid artery wall thickness, compatible with their putatively atherogenic and antiatherogenic properties.

Black or African American↗

PubMed2000

Nutrient intakes and dietary patterns of young children by dietary fat intakes.

OBJECTIVE: To determine whether low fat intake is associated with increased risk of nutritional inadequacy in children 2 to 8 years old and to identify eating patterns associated with differences in fat intake. STUDY DESIGN: Using 2 days of recall from the Continuing Survey of Food Intake by Individuals (CSFII), 1994 to 1996, we classified 2802 children into quartiles of energy intake from fat (<29%, 29% to 31.9% [defined as moderate fat], 32% to 34.9%, and > or =35%) and compared nutrient intakes, the proportion of children at risk for inadequate intakes, Food Pyramid servings, and fat content per serving across quartiles. RESULTS: More children in quartile 2 were at risk for inadequate intakes of vitamin E, calcium, and zinc than children in higher quartiles (P <.0001); more children in quartiles 3 and 4 were at risk for inadequate intakes of vitamins A and C and folate (P <.001). Fruit intake decreased across quartiles (P <.0001); whereas vegetable, meat, and fat-based condiment intakes increased (P <.0001). Fat per serving of grain, vegetables, dairy, and meat increased across quartiles (P <.0001). CONCLUSIONS: Moderate-fat diets were not consistently associated with an increased proportion of children at risk for nutritional inadequacy, and higher-fat diets were not consistently protective against inadequacy. Dietary fat could be reduced by judicious selection of lower-fat foods without compromising nutritional adequacy.

Child↗

PubMed1986

Effects of type of dietary fat and carbohydrate on gluconeogenesis in isolated hepatocytes from BHE rats.

The effect of type of dietary fat and carbohydrate on gluconeogenesis and ketogenesis by isolated hepatocytes was studied. BHE male weanling rats were fed one of six diets: 64% sucrose or cornstarch with 6% corn oil, 6% hydrogenated coconut oil, or a 1:2 mixture of the two oils. At 100 d of age the rats were anesthetized, and isolated hepatocytes were prepared. The cells were incubated with lactate, lactate and lysine, lactate and pyruvate, lactate and palmitate, lactate and linoleate, lactate and epinephrine or lactate and glucagon. The hepatocytes from the rats that had been fed hydrogenated coconut oil produced significantly more glucose than the rats fed either corn oil or a mixture of oils, regardless of the type of carbohydrate fed. Each of the additives in turn, except for epinephrine, stimulated glucose production above that obtained with lactate alone. However, when expressed as a percent increase above that from lactate there was no effect of fat type on the magnitude of this stimulation. We interpret these data to mean that, although the metabolic pathways function equally well in the hepatocytes isolated from rats fed hydrogenated coconut oil and rats fed corn oil, the flux through these pathways can be influenced by the type of dietary fat.

Animals↗

PubMed1988

Relation of changes in amount and type of dietary fat to fecapentaenes in premenopausal women.

Correlation studies suggest that fecal mutagenicity is increased in groups eating high-fat diets, the same groups who are often found to have high colorectal cancer incidence and mortality. The fecapentaenes are the best characterized class of fecal mutagens, but the relationship of dietary fat intake to the excretion of these potent genotoxins is unknown. We studied the effect of changes in amount and type of dietary fat on fecapentaene levels in 31 premenopausal women 20-40 years of age who participated in a controlled feeding study. After a pre-diet free-living period lasting 1 menstrual cycle, women were placed on a high-fat (40% energy from fat) diet for 4 menstrual cycles and then switched to a low-fat (20% energy from fat) diet for an additional 4 menstrual cycles. One-half the subjects were maintained throughout the study at a ratio of polyunsaturated-to-saturated fatty acids (P/S ratio) of 1.0, the other half at 0.3; body weight was constant. All meals during the controlled diet periods were prepared at the Human Study Facility of the Beltsville Human Nutrition Research Center. Fecapentaene and fecapentaene precursor levels were measured in acetone extracts from 3-day pooled stool samples collected during the study. No differences in fecapentaene or precursor levels were observed between the high- and low-fat diets at either P/S ratio. Fecapentaene and precursor levels were higher while on controlled diets than during the pre-diet free-living period, and levels declined again in the post-diet free-living period. We conclude that dietary fat has no significant effect on fecapentaene or precursor levels in acetone extracts of stool in premenopausal women. The effect of other dietary or non-dietary factors on fecapentaenes remains unknown.

Adult↗

PubMed1985

Dietary fat consumption and survival among women with breast cancer.

An historical prospective study was conducted to examine the relationship of dietary fat intake to disease progression and length of survival of 953 women with breast cancer. Estimates of monthly fat intake were based on patient responses about usual frequency of consuming 33 foods and beverages prior to symptom onset. Average estimated monthly fat intake did not vary by stage of disease at diagnosis. When controlling for disease stage and patient age at diagnosis, the estimated risk of death at any time increased 1.4-fold for each 1,000 g in monthly fat intake. Separate analysis by disease stage showed this association to be most pronounced for subjects with advanced disease. The need for future studies to incorporate clinical and pathologic factors in the analysis, to distinguish between sources of dietary fat intake, and to ascertain dietary patterns subsequent to breast cancer diagnosis was noted.

Adult↗

PubMed2006

Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.

CONTEXT: Observational studies and polyp recurrence trials are not conclusive regarding the effects of a low-fat dietary pattern on risk of colorectal cancer, necessitating a primary prevention trial. OBJECTIVE: To evaluate the effects of a low-fat eating pattern on risk of colorectal cancer in postmenopausal women. DESIGN, SETTING, AND PARTICIPANTS: The Women's Health Initiative Dietary Modification Trial, a randomized controlled trial conducted in 48,835 postmenopausal women aged 50 to 79 years recruited between 1993 and 1998 from 40 clinical centers throughout the United States. INTERVENTIONS: Participants were randomly assigned to the dietary modification intervention (n = 19,541; 40%) or the comparison group (n = 29,294; 60%). The intensive behavioral modification program aimed to motivate and support reductions in dietary fat, to increase consumption of vegetables and fruits, and to increase grain servings by using group sessions, self-monitoring techniques, and other tailored and targeted strategies. Women in the comparison group continued their usual eating pattern. MAIN OUTCOME MEASURE: Invasive colorectal cancer incidence. RESULTS: A total of 480 incident cases of invasive colorectal cancer occurred during a mean follow-up of 8.1 (SD, 1.7) years. Intervention group participants significantly reduced their percentage of energy from fat by 10.7% more than did the comparison group at 1 year, and this difference between groups was mostly maintained (8.1% at year 6). Statistically significant increases in vegetable, fruit, and grain servings were also made. Despite these dietary changes, there was no evidence that the intervention reduced the risk of invasive colorectal cancer during the follow-up period. There were 201 women with invasive colorectal cancer (0.13% per year) in the intervention group and 279 (0.12% per year) in the comparison group (hazard ratio, 1.08; 95% confidence interval, 0.90-1.29). Secondary analyses suggested potential interactions with baseline aspirin use and combined estrogen-progestin use status (P = .01 for each). Colorectal examination rates, although not protocol defined, were comparable between the intervention and comparison groups. Similar results were seen in analyses adjusting for adherence to the intervention. CONCLUSION: In this study, a low-fat dietary pattern intervention did not reduce the risk of colorectal cancer in postmenopausal women during 8.1 years of follow-up. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.

Adenoma↗

PubMed1981

Effects of the type of dietary fat at two levels of vitamin E in Wistar male rats during development and aging. III. Biochemical and morphometric parameters of the liver.

The purpose of this study was to explore in rats the possible influence of the type of dietary fat at two extreme levels of vitamin E on several biochemically determined hepatic changes and on a number of quantitatively analyzed structural and ultrastructural variations with age in hepatic cells. Six groups of weanling Wistar male rats were fed ad libitum isoenergetic diets containing similar amounts (15 g per 100 g diet) of saturated fat (coconut oil), unsaturated fat (safflower oil) or a combination of both at two levels of dl-alpha-tocopherol (2 or 200 mg per 100 g of diet). Determinations were performed in rats killed at 3, 6, 12, 18 and 24 months. Although in relation to age and irrespective of the type of diet, several of the biochemical parameters fluctuated with time, comparisons of the results between the youngest and oldest rats showed no changes in the levels of hepatic RNA, phospholipids, cholesterol, total tocopherols and total collagens, significant increases in DNA and triglycerides and a significant decrease in total protein. While the type of diet did not have in general significant influences on the levels of DNA, RNA, total protein and collagens, either the type of dietary fat and/or the levels of vitamin E had some definite effects on the levels of triglycerides, cholesterol, phospholipids and total tocopherols, as well as on the in vitro formation of malonaldehyde and on the eventual occurrence of in vivo lipoperoxidation (diene conjugation). These effects, however, varied in relation to the duration of the diverse dietary treatments. The morphologic studies indicated that all the livers had variable but generally moderate degrees of fatty changes (mainly due to triglyceride accumulation) which were attributed to the moderate obesity found in the rats. The mean nuclear and cell dimensions of hepatocytes, the number of binucleated hepatocytes, surface density of rough endoplasmic reticulum, numerical density of mitochondria and the fractional cytoplasmic volume occupied by lipofuscin pigment in hepatocytes were not significantly affected by the type of diet, by age or by the eventual occurrence of in vivo hepatic lipoperoxidation, whereas the numerical density of hepatocytes (mono- and binucleated) and "litoral cells" (endothelial, Kupffer and Ito cells), although unaffected by diet, significantly increased with age. On the other hand, the fractional volume of mitochondria and peroxisomes, as well as the numerical density of peroxisomes, were significantly influenced by the type of dietary fat and to lesser extent by the dietary levels of vitamin E.

Aging↗

PubMed1990

Analysis of dietary fat, calories, body weight, and the development of mammary tumors in rats and mice: a review.

We have extracted from the literature data from 100 animal experiments, involving 7838 rats and mice, which compared the effects of different levels of dietary fat and/or calorie intake on the development of mammary tumors. Both higher calorie intake (P less than 0.0001) and higher fat intake (P less than 0.0001) independently increased mammary tumor incidence in Sprague-Dawley rats and in mice, as judged from analyses combining ad libitum feeding experiments and restricted feeding experiments. The effect of fat was two thirds the magnitude of the calorie effect in both Sprague-Dawley rats and mice. In ad libitum feeding experiments, a modest but significant (P less than 0.0001) average increase in body weight was found in animals fed high fat diets. However, these differences in body weight did not correspond to differences in mammary tumor incidence. The effect of log body weight on the log odds of tumor incidence was not significant (P = 0.16), while dietary fat intake significantly increased tumor incidence (P less than 0.0001). The collection of animal experimental data supports the hypothesis that, in mammary tumor development, there is a specific enhancing effect of dietary fat, as well as a general enhancing effect of calories.

Animals↗

PubMed2004

A solid dietary fat containing fish oil redistributes lipoprotein subclasses without increasing oxidative stress in men.

There is a demand and need for healthy solid dietary fats. However, synthetic fats can be tailored to contain specific physiologic properties. Our goal was to design dietary solid test fats that would be both beneficial to the atherogenic lipid profile and stable against lipid peroxidation. Sixteen men (age 35-75 y) substituted 80 g of their normal dietary fat intake with test fat for two periods of 21 d each in a double-blind, randomized, crossover study. Although solid, both test fats were low in cholesterol-raising SFA. Test fat "F" contained 5 g/100 g long chain (n-3) fatty acids matched by oleic acid in test fat "O." Plasma total triacylglycerol (TAG), VLDL TAG, cholesterol in VLDL, and intermediate density lipoproteins (IDL) were lower (P < 0.05), whereas apolipoprotein (apo) B of the large LDL-2 (d = 1031-1042 g/L) subclass, and cholesterol of HDL(2b) subclass, were higher after intake of F than O fat (P < 0.05). There was no difference in the effect on in vivo oxidation measured as the ratio of plasma isoprostanes F(2) to arachidonic acid and urinary isoprostanes, whereas the vitamin E activity/plasma total lipids ratio was higher after intake of F than O (P = 0.008). In conclusion, a solid dietary fat containing (n-3) PUFA decreased plasma TAG, VLDL, and IDL cholesterol, and redistributed lipoprotein subclasses in LDL and HDL, with a higher concentration of the larger and less atherogenic subfractions. These changes took place without an increase in oxidative stress as measured by in vivo markers.

Adult↗

PubMed2006

Enterostatin inhibition of dietary fat intake is modulated through the melanocortin system.

Enterostatin injected into the amygdala selectively reduces dietary fat intake by an action that involves a serotonergic component in the paraventricular nucleus. We have investigated the role of melanocortin signaling in the response to enterostatin by studies in melanocortin 4 receptor (MC4R) knock out mice and by the use of the MC4R and MC3R antagonist SHU9119, and by neurochemical phenotyping of enterostatin activated cells. We also determined the effect of enterostatin in vivo on the expression of AgRP in the hypothalamus and amygdala of rats and in culture on a GT1-7 neuronal cell line. Enterostatin had no effect on food intake in MC4R knock out mice. SHU9119 i.c.v. blocked the feeding response to amygdala enterostatin in rats. Amygdala enterostatin induced fos activation in alpha-melanocyte stimulating hormone (alpha-MSH) neurons in the arcuate nucleus. Enterostatin also reduced the expression of AgRP in the hypothalamus and amygdala and in GT1-7 cells. These data suggest enterostatin inhibits dietary fat intake through a melanocortin signaling pathway.

Agouti-Related Protein↗