Dietary gamma-linolenic acid in the form of borage oil causes less body fat accumulation accompanying an increase in uncoupling protein 1 mRNA level in brown adipose tissue

Rats were fed a low-fat diet containing 2% safflower oil or 20% fat diets containing either safflower oil rich in linoleic acid, borage oil containing 25% gamma (gamma)-linolenic acid or enzymatically prepared gamma-linolenic acid enriched borage oil containing 47% gamma-linolenic acid for 14 days. Energy intake and growth of animals were the same among groups. A high safflower oil diet compared with a low-fat diet caused significant increases in both epididymal and perirenal white adipose tissue weights. However, high-fat diets rich in gamma-linolenic acid failed to do so. Compared with a low-fat diet, all the high-fat diets increased mRNA levels of uncoupling protein 1 and lipoprotein lipase in brown adipose tissue. The extents of the increase were greater with high-fat diets rich in gamma-linolenic acid. Various high-fat diets, compared with a low-fat diet, decreased glucose transporter 4 mRNA in white adipose tissue to the same levels. The amount and types of dietary fat did not affect the leptin mRNA level in epididymal white adipose tissue. However, a high safflower oil diet, but not high-fat diets rich in gamma-linolenic acid relative to a low-fat diet, increased perirenal white adipose tissue leptin mRNA levels. All high-fat diets, relative to a low-fat diet, increased the hepatic mitochondrial fatty acid oxidation rate and fatty acid oxidation enzyme mRNA abundances to the same levels. High-fat diets also increased these parameters in the peroxisomal pathway, and the increases were greater with high-fat diets rich in gamma-linolenic acid. The physiological activity in increasing brown adipose tissue gene expression and peroxisomal fatty acid oxidation was similar between the two types of borage oil differing in gamma-linolenic acid content. It was suggested that dietary gamma-linolenic acid attenuates body fat accumulation through the increase in gene expressions of uncoupling protein 1 in brown adipose tissue. An increase in hepatic peroxisomal fatty acid oxidation may also contribute to the physiological activity of gamma-linolenic acid in decreasing body fat mass.     

Fecapentaenes and their precursors throughout the bowel--results of an autopsy study

The fecapentaenes are potent mutagens found in the stool of some humans and pigs. These compounds are produced by Bacteroides species in the gut from an uncharacterized family of precursor compounds, and have been postulated to pose a risk of human colorectal cancer. To better understand fecapentaene production in vivo, and to determine if excreted levels measured in epidemiologic studies are representative of the entire colon, fecapentaenes were assayed from multiple sites in the bowel in an autopsy study of 16 humans and 2 pigs. An indirect measurement of fecapentaene precursors was also made. Colonic concentrations of fecapentaenes and precursors varied widely between individuals, but were consistent for each individual throughout the colon. In addition, the measurements of rectal contents, assumed to approximate values in excreted stool, were equivalent to measurements from the colon.     

Body Fat Accumulation in Zebrafish Is Induced by a Diet Rich in Fat and Reduced by Supplementation with Green Tea Extract

Fat-rich diets not only induce obesity in humans but also make animals obese. Therefore, animals that accumulate body fat in response to a high-fat diet (especially rodents) are commonly used in obesity research. The effect of dietary fat on body fat accumulation is not fully understood in zebrafish, an excellent model of vertebrate lipid metabolism. Here, we explored the effects of dietary fat and green tea extract, which has anti-obesity properties, on body fat accumulation in zebrafish. Adult zebrafish were allocated to four diet groups and over 6 weeks were fed a high-fat diet containing basal diet plus two types of fat or a low-fat diet containing basal diet plus carbohydrate or protein. Another group of adult zebrafish was fed a high-fat diet with or without 5% green tea extract supplementation. Zebrafish fed the high-fat diets had nearly twice the body fat (visceral, subcutaneous, and total fat) volume and body fat volume ratio (body fat volume/body weight) of those fed low-fat diets. There were no differences in body fat accumulation between the two high-fat groups, nor were there any differences between the two low-fat groups. Adding green tea extract to the high-fat diet significantly suppressed body weight, body fat volume, and body fat volume ratio compared with the same diet lacking green tea extract. 3-Hydroxyacyl-coenzyme A dehydrogenase and citrate synthase activity in the liver and skeletal muscle were significantly higher in fish fed the diet supplemented with green tea extract than in those fed the unsupplemented diet. Our results suggest that a diet rich in fat, instead of protein or carbohydrate, induced body fat accumulation in zebrafish with mechanisms that might be similar to those in mammals. Consequently, zebrafish might serve as a good animal model for research into obesity induced by high-fat diets.     

Laboratory and epidemiologic studies of fecapentaenes

Fecapentaenes are a class of conjugated ether lipids which have been identified as the major component of human fecal mutagenicity in the Ames Salmonella mutagenesis assay. Human epidemiologic data have indicated that most healthy North American populations eating a western diet do excrete detectable levels of fecapentaenes. Excreted fecapentaene levels seem to reflect levels throughout the colonic lumen, and levels vary characteristically between individuals. Those individuals found to excrete high levels of fecapentaene appear, based on limited data, to be at decreased risk of colorectal neoplasia. Carcinogenicity studies in rats and mice have been predominantly negative, however, increased tumor incidence in mice exposed to fecapentaenes as neonates has recently been reported. Fecapentaenes are direct-acting genotoxins, which may react with DNA through free radical mechanisms, and/or aldehyde formation. Mechanisms by which fecapentaene-induced DNA damage may mediate carcinogenesis are discussed.     

Levels of 5-hydroxymethyl-2'-deoxyuridine in DNA from women participating in an intervention trial of low-fat and low-energy diets

Oxidative DNA damage in blood appears to be useful as a marker of systemic oxidative stress levels. Dietary factors such as fat and energy intakes have been indicated to affect oxidative stress levels, and this may be an important mechanism by which diet can modulate cancer risk. The primary objective of this study was to investigate the effects of dietary intervention in premenopausal women on the levels of one type of oxidative DNA damage: 5-hydroxymethyl-2'-deoxyuridine. The trial randomly assigned women to control, low-fat, low-energy or combination low-fat/low-energy diets for 12 weeks. Blood samples were obtained every 2 weeks, and DNA was analysed for the levels of 5-hydroxymethyl-2'-deoxyuridine. Levels of DNA damage declined with time in each diet arm, including the control arm. The decreases were greater in the two arms with low-energy intake, but not significantly so. The numbers of women who exhibited decreased 5-hydroxymethyl-2'-deoxyuridine levels at 12 weeks versus baseline levels, however, was significantly greater in women assigned to any intervention diet (79%) than in the control arm (50%). Low-fat and low-energy diets therefore had a small effect on changes in oxidative DNA damage levels. The women participating in this study were not selected on the basis of increased cancer risk; therefore, they may have had low baseline levels of damage that were not amenable to further reduction by dietary change.     

Stimulation of fecal fat excretion and the disposal of protoporphyrin in a murine model for erythropoietic protoporphyria

Erythropoietic protoporphyria (EPP) is characterized by toxic accumulation of the hydrophobic compound protoporphyrin (PP). Ferrochelatase-deficient (fch/fch) mice are an animal model for human EPP. Recently, we have demonstrated that the accumulation of another hydrophobic compound, unconjugated bilirubin, could effectively be treated by stimulation of fecal fat excretion. We investigated whether stimulation of fecal fat excretion enhanced the disposal of PP in fch/fch mice. Fch/fch mice were fed for 8 wk with a high-fat diet (16 wt% fat; control) or with the high-fat diet mixed with either a nonabsorbable fat (sucrose polyester) or the intestinal lipase inhibitor orlistat. The effects of the treatments on fecal excretion of fat and PP and on hepatic PP concentrations were compared with control diets. Fecal fat excretion in fch/fch mice on a high-fat diet was higher than in mice on a low-fat diet (+149%, P < 0.05). Sucrose polyesters and orlistat increased fecal fat excretion even more, up to sixfold of control values. However, none of the different treatments affected fecal PP excretion or hepatic PP concentration. Treatment of fch/fch mice with a high-fat diet, a nonabsorbable fat diet, or with orlistat increased the fecal excretion of fat but did not increase fecal PP excretion or decrease hepatic PP concentration. The present data indicate that accumulation of PP is not amenable to stimulation of fecal fat excretion.     

Dietary fat and immune function. II. Effects on immune complex nephritis in (NZB x NZW)F1 mice

(NZB x NZW)F1 mice initiated on fat restriction at weanling were significantly protected from the development of immune complex glomerulonephritis. Whereas the mice on high-fat intake demonstrated immune depositions both in capillary walls and mesangial areas in a diffuse granular pattern, those on a low-fat diet with caloric content similar to the high-fat diets exhibited mesangial confinement of the depositions of immunoglobulins, complement, and retroviral gp70. In association with these divergent patterns of immune deposition, the mice on high-fat diets had evidence of extensive diffuse cellular proliferation, wire loop lesion, and sclerosis in the glomeruli. In contrast, most of the mice on the low-fat diet showed only mesangial cell and matrix proliferations. In addition, the group of mice fed high saturated fat showed more severe glomerular pathology as compared to those fed high unsaturated fat. Paradoxically, levels of circulating immune complexes (as measured by the polyethylene glycol precipitation technique) in the high saturated fat group were low and did not correlate with the findings by light and immunofluorescence microscopy. These findings suggest that dietary fat restriction can serve as either a prophylactic or effective therapeutic approach to murine lupus nephritis.     

Failure of high dietary fat to influence serum prolactin levels during the estrous cycle in female Sprague-Dawley rats

The influence of a 20% high-fat and a 4.5% control fat diet on circulating prolactin levels was determined during the estrous cycle of intact female rats, and during a progesterone-induced surge of prolactin in ovariectomized, estrogen-primed rats. An indwelling right atrial cannula was implanted into each rat to facilitate repeated blood sampling in conscious, undisturbed animals. No differences in serum prolactin levels were observed at any time during the estrous cycle or in the progesterone-induced surge of prolactin in rats fed either the high-fat or control fat diet. There also were no differences in the estrous cycles of rats on high- or low-fat diets. It is concluded that high dietary fat promotes mammary tumor development by a mechanism that does not involve alterations in circulating prolactin levels or of estrous cycles.     

Levels of 5-hydroxymethyl-2′-deoxyuridine in DNA from women participating in an intervention trial of low-fat and low-energy diets

Oxidative DNA damage in blood appears to be useful as a marker of systemic oxidative stress levels. Dietary factors such as fat and energy intakes have been indicated to affect oxidative stress levels, and this may be an important mechanism by which diet can modulate cancer risk. The primary objective of this study was to investigate the effects of dietary intervention in premenopausal women on the levels of one type of oxidative DNA damage: 5-hydroxymethyl-2′-deoxyuridine. The trial randomly assigned women to control, low-fat, low-energy or combination low-fat/low-energy diets for 12?weeks. Blood samples were obtained every 2?weeks, and DNA was analysed for the levels of 5-hydroxymethyl-2′-deoxyuridine. Levels of DNA damage declined with time in each diet arm, including the control arm. The decreases were greater in the two arms with low-energy intake, but not significantly so. The numbers of women who exhibited decreased 5-hydroxymethyl-2′-deoxyuridine levels at 12?weeks versus baseline levels, however, was significantly greater in women assigned to any intervention diet (79%) than in the control arm (50%). Low-fat and low-energy diets therefore had a small effect on changes in oxidative DNA damage levels. The women participating in this study were not selected on the basis of increased cancer risk; therefore, they may have had low baseline levels of damage that were not amenable to further reduction by dietary change.     

Acute changes in the response to peripheral leptin with alteration in the diet composition

Dietary induced obesity in rodents is associated with a resistance to leptin. We have investigated the hypothesis that dietary fat per se alters the feeding response to peripheral leptin in rats that were fed either their habitual high- or low-fat diet or were naively exposed to the alternative diet. Osborne-Mendel rats were adapted to either high- or low-fat diet. Food-deprived rats were given either leptin (0.5 mg/kg body wt ip) or saline, after which they were provided with either their familiar diet or the alternative diet. Food intake of rats adapted and tested with the low-fat diet was reduced 4 h after leptin injection, whereas rats adapted and tested with a high-fat diet did not respond to leptin. Leptin was injected again 1 and 5 days after the high-fat diet-adapted rats were switched to the low-fat diet. Leptin reduced the food intake on both days. In contrast, when low-fat diet-adapted rats were switched to a high-fat diet, the leptin inhibitory response was present on day 1 but not observed on day 5. Peripheral injection of leptin increased serum corticosterone level and decreased hypothalamic neuropeptide Y mRNA expression in rats fed the low-fat but not the high-fat diet for 20 days. The data suggest that dietary fat itself, rather than obesity, may induce leptin resistance within a short time of exposure to a high-fat diet.     

Sex differences in the response of postprandial lipemia to a change from a low-fat low-cholesterol diet to a high-fat high-cholesterol diet

To determine whether a short-term change in dietary habits affects postprandial lipemia in men and women in the same way, postprandial triglyceridemia was measured in age- and BMI-matched young healthy men and women after two weeks on the self-selected low-fat low-cholesterol (LF) diet and after another two weeks on the self-selected high-fat high-cholesterol (HF) diet. After a standardized challenge meal (1.4 g fat/kg of body weight), men had higher postprandial triglyceridemia than women on the HF diet but no such difference was observed on the LF diet. The results of this preliminary study suggest that there may be important sex differences in the mechanisms regulating the postprandial lipemia response to different diets, women being able to adapt better to the HF diet with respect to postprandial lipemia.     

Influence of dietary fat on the promotion of diethylnitrosamine-induced hepatocarcinogenesis in female rats

The effect of varying the amount and type of dietary fat on the promotion of gamma-glutamyltranspeptidase (GGT)-positive foci and hepatocarcinomas in female rats was studied. In the first study, two-thirds of the rats were first intubated with diethylnitrosamine (DEN, 10 mg/kg) 20 hr after partial hepatectomy; 1 week later, rats were fed one of three purified diets (a low-fat diet similar to the AIN-76 diet, a high saturated fat diet, or a high polyunsaturated fat diet) with or without 0.05% phenobarbital in the diet for 10 months. Increasing the fat level of the diet did not increase the number of GGT-positive foci arising spontaneously or induced by DEN alone. When phenobarbital was present in the diet, feeding the high polyunsaturated fat diet slightly increased the number of GGT-positive foci and the incidence of tumors. The low-fat diet, however, increased the incidence of fatty liver. We therefore reexamined the effect of diet on promotion by phenobarbital, using an additional low-fat diet with cornstarch rather than sucrose as the carbohydrate source. In this experiment, both high-fat diets slightly enhanced the induction of GGT-positive foci; the carbohydrate source had no effect. The incidence of tumors was not affected by diet in this experiment, but the incidence of fatty liver was again enhanced by feeding a diet high in sucrose. We conclude that increasing the fat level of the diet does not promote the development of DEN-initiated GGT-positive foci or carcinomas in female rats. Increasing the dietary fat level, however, may enhance promotion of liver foci by phenobarbital. Finally, increasing the sucrose content of the diet increases the incidence of fatty liver.     

Effect of high-fat diet during gestation, lactation, or postweaning on physiological and behavioral indexes in borderline hypertensive rats

Maternal obesity is becoming more prevalent. We used borderline hypertensive rats (BHR) to investigate whether a high-fat diet at different stages of development has adverse programming consequences on metabolic parameters and blood pressure. Wistar dams were fed a high- or low-fat diet for 6 wk before mating with spontaneously hypertensive males and during the ensuing pregnancy. At birth, litters were fostered to a dam from the same diet group as during gestation or to the alternate diet condition. Female offspring were weaned on either control or "junk food" diets until about 6 mo of age. Rats fed the high-fat junk food diet were hyperphagic relative to their chow-fed controls. The junk food-fed rats were significantly heavier and had greater fat pad mass than those rats maintained on chow alone. Importantly, those rats suckled by high-fat dams had heavier fat pads than those suckled by control diet dams. Fasting serum leptin and insulin levels differed as a function of the gestational, lactational, and postweaning diet histories. Rats gestated in, or suckled by high-fat dams, or maintained on the junk food diet were hyperleptinemic compared with their respective controls. Indirect blood pressure did not differ as a function of postweaning diet, but rats gestated in the high-fat dams had lower mean arterial blood pressures than those gestated in the control diet dams. The postweaning dietary history affected food-motivated behavior; junk food-fed rats earned less food pellets on fixed (FR) and progressive (PR) ratio cost schedules than chow-fed controls. In conclusion, the effects of maternal high-fat diet during gestation or lactation were mostly small and transient. The postweaning effects of junk food diet were evident on the majority of the parameters measured, including body weight, fat pad mass, serum leptin and insulin levels, and operant performance.     

Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides

The opioid peptides enkephalin (ENK) and dynorphin (DYN), when injected into the hypothalamus, are known to stimulate feeding behavior and preferentially increase the ingestion of a high-fat diet. Studies of another peptide, galanin (GAL), with similar effects on feeding demonstrate that a high-fat diet, in turn, can stimulate the expression of this peptide in the hypothalamus. The present study tested different diets and variable periods of high- vs. low-fat diet consumption to determine whether the opioid peptides respond in a similar manner as GAL. In six experiments, the effects of dietary fat on ENK and DYN were examined in three hypothalamic areas: the paraventricular nucleus (PVN), perifornical hypothalamus (PFH), and arcuate nucleus (ARC). The results demonstrated that the ingestion of a high-fat diet increases gene expression and peptide levels of both ENK and DYN in the hypothalamus. The strongest and most consistent effect is seen in the PVN. In this nucleus, ENK and DYN are increased by 50-100% after 1 wk, 1 day, 60 min, and even 15 min of high-fat diet consumption. While showing some effect in the PFH, these peptides in the ARC are considerably less responsive, exhibiting no change in response to the briefer periods of diet intake. This effect of dietary fat on PVN opioids can be observed with diets equal in caloric density and palatability and without a change in caloric intake, body weight, fat pad weight, or levels of insulin or leptin. The data reveal a strong and consistent association between these peptides and a rise in circulating levels of triglycerides, supporting a role for these lipids in the fat-induced stimulation of opioid peptides in the PVN, similar to GAL.     

Effects of dietary fat types on body fatness,leptin, and ARC leptin receptor,NPY, and AgRP mRNA expression

Some, but not all, fats are obesogenic. The aim of the present studies was to investigate the effects of changing type and amount of dietary fats on energy balance, fat deposition, leptin, and leptin-related neural peptides: leptin receptor, neuropeptide Y (NPY), agouti-related peptide (AgRP), and proopiomelanocortin (POMC), in C57Bl/6J mice. One week of feeding with a highly saturated fat diet resulted in ~50 and 20% reduction in hypothalamic arcuate NPY and AgRP mRNA levels, respectively, compared with a low-fat or an n-3 or n-6 polyunsaturated high-fat (PUFA) diet without change in energy intake, fat mass, plasma leptin levels, and leptin receptor or POMC mRNA. Similar neuropeptide results were seen at 7 wk, but by then epididymal fat mass and plasma leptin levels were significantly elevated in the saturated fat group compared with low-fat controls. In contrast, fat and leptin levels were reduced in the n-3 PUFA group compared with all other groups. At 7 wk, changing the saturated fat group to n-3 PUFA for 4 wk completely reversed the hyperleptinemia and increased adiposity and neuropeptide changes induced by saturated fat. Changing to a low-fat diet was much less effective. In summary, a highly saturated fat diet induces obesity without hyperphagia. A regulatory reduction in NPY and AgRP mRNA levels is unable to effectively counteract this obesogenic drive. Equally high fat diets emphasizing PUFAs may even protect against obesity.     

Growth hormone-mediated breakdown of body fat: effects of GH on lipases in adipose tissue and skeletal muscle of old rats fed different diets.

Lipid storage and breakdown is mainly controlled by lipoprotein lipase and hormone-sensitive lipase. The aim of this work was to elucidate whether growth hormone mediated loss of adipose tissue involves a concerted action on tissue lipases, and to what degree such events are modulated by dietary regimen. Twelve-month-old rats fed first a high-fat diet or a low-fat diet for 14 weeks were injected with saline or growth hormone (4 mg/kg/d) for four days or three weeks in different combinations with either high- or low-fat diets. In adipose tissue, growth hormone generally inhibited lipoprotein lipase and also attenuated the inhibiting effect of insulin on hormone-sensitive lipase activity. Growth hormone treatment combined with restricted high-fat feeding reduced the activity of both lipases in adipose tissue and stimulated hormone-sensitive lipase in muscle. Generally, plasma levels of free fatty acids, glycerol and cholesterol were reduced by growth hormone, and in combination with restricted high-fat feeding, triglyceride levels improved too. We conclude that growth hormone inhibits lipid storage in adipose tissue by reducing both lipoprotein lipase activity and insulin's inhibitory action on hormone-sensitive lipase. We also propose that growth hormone's effects on tissue lipases and blood lipids are modulated by dietary regimen.     

Decreasing Effect of Chitosan on the Apparent Fat Digestibility by Rats Fed on a High-fat Diet

We investigated the effects of various dietary fibers or their likenesses on the apparent fat digestibility by rats fed on a high-fat diet. Each of 23 different fibers was added at 5% (w/w) to a purified diet containing 20% (w/w) corn oil. The rats were fed these diets for 2 weeks, and the feces were collected from each animal during the last 3 days. When compared with cellulose (control), 10 of the tested fibers significantly increased the fecal lipid excretion. Among these fibers, chitosan markedly increased the fecal lipid excretion and reduced the apparent fat digestibility to about a half relative to the control. The apparent protein digestibility was not greatly affected by chitosan. The fatty acid composition of the fecal lipids closely reflected that of the dietary fat. These results suggest that chitosan has potency for interfering with fat digestion and absorption in the intestinal tract, and for facilitating the excretion of dietary fat into the feces.     

Ventromedial Hypothalamic NPY Y2 Receptor in the Maintenance of Body Weight in Diet-Induced Obesity in Mice

This study examined changes in neuropeptide Y (NPY) Y2 receptor binding in the brains of C57BL/6 mice in response to different levels of high-fat diets via three dietary intervention methods: high-fat diet, switching from high- to low-fat diet and finally, energy restricted high-fat diet. Forty-five C57Bl/6 male mice were fed a high-fat diet for 8 weeks and then classified as diet-induced obese (DIO) or diet-resistant (DR) mice according to the highest and lowest body weight gainers, respectively. The DIO and DR mice were then randomly divided into three groups each and either continued on their high-fat diet ad libitum (DIO-H and DR-H), changed to a low-fat diet (DIO-L and DR-L) or pair-fed via energy restricted high-fat diet (DIO-P and DR-P) for a further 6 weeks. During the course of this study, body weight, energy intake and plasma peptide YY (PYY) were measured. The study revealed that the replacement of a high-fat diet with a low-fat diet was associated with a significant lowering of ventromedial hypothalamic (VMH) Y2 receptor binding in both the DIO-L and DR-L mice (−37%, −36%), and also a lowered plasma PYY level in the DIO-L mice (−25%). Despite a continued consumption of the high-fat diet, energy restricted pair feeding caused a lower VMH Y2 receptor binding in the obese mice (DIO-P) following weight loss compared to the DR-P mice (−14%). In conclusion, this study showed that changing diets from high- to low-fat can significantly lower the VMH Y2 receptor binding irrespective to the obesity phenotype. Energy restriction, even while on high-fat feeding, can cause a lower VMH Y2 receptor binding compared to DR mice even after body weight loss to similar levels. This suggests either a possible intrinsic nature of the DIO mice or a body weight set-point re-establishment to drive body weight regain.     

High-Fat Diet Reduces the Formation of Butyrate,but Increases Succinate,Inflammation, Liver Fat and Cholesterol in Rats,while Dietary Fibre Counteracts These Effects

Introduction

Obesity is linked to type 2 diabetes and risk factors associated to the metabolic syndrome. Consumption of dietary fibres has been shown to have positive metabolic health effects, such as by increasing satiety, lowering blood glucose and cholesterol levels. These effects may be associated with short-chain fatty acids (SCFAs), particularly propionic and butyric acids, formed by microbial degradation of dietary fibres in colon, and by their capacity to reduce low-grade inflammation.

Objective

To investigate whether dietary fibres, giving rise to different SCFAs, would affect metabolic risk markers in low-fat and high-fat diets using a model with conventional rats for 2, 4 and 6 weeks.

Material and Methods

Conventional rats were administered low-fat or high-fat diets, for 2, 4 or 6 weeks, supplemented with fermentable dietary fibres, giving rise to different SCFA patterns (pectin – acetic acid; guar gum – propionic acid; or a mixture – butyric acid). At the end of each experimental period, liver fat, cholesterol and triglycerides, serum and caecal SCFAs, plasma cholesterol, and inflammatory cytokines were analysed. The caecal microbiota was analysed after 6 weeks.

Results and Discussion

Fermentable dietary fibre decreased weight gain, liver fat, cholesterol and triglyceride content, and changed the formation of SCFAs. The high-fat diet primarily reduced formation of SCFAs but, after a longer experimental period, the formation of propionic and acetic acids recovered. The concentration of succinic acid in the rats increased in high-fat diets with time, indicating harmful effect of high-fat consumption. The dietary fibre partly counteracted these harmful effects and reduced inflammation. Furthermore, the number of Bacteroides was higher with guar gum, while noticeably that of Akkermansia was highest with the fibre-free diet.     

Comparison of Osborne-Mendel and S5B/PL Strains of Rat: Central Effects of Galanin,NPY, β-Casomorphin and CRH on Intake of High-Fat and Low-Fat Diets

The effects of central administration of galanin, neuropeptide Y (NPY), β-casomorphin_(1–7) and corticotropin releasing hormone (CRH) on intake of either a high-fat or low-fat diet have been compared in two strains of rat, the dietary fat-sensitive Osborne-Mendel (OM) rat and the dietary fat-resistant S5B/Pl rat. Injection of galanin (0.1, 0.3 nmoles) into the 3rd cerebral ventricle stimulated the intake of both a high-fat and a low-fat diet in OM rats in a dose dependent manner but the response was significantly smaller in rats fed the low-fat diet. In S5B/Pl rats, galanin had a small stimulatory effect on food intake but only at a high dose (2 nmole). β-casomor-phin_(1–7) (5 nmoles), an opioid-like peptide, increased the intake of the high-fat but not the low-fat diet in OM rats, whereas S5B/Pl rats fed either a high-fat or a low-fat diet did not respond to β-caso-morphin/j.yy Both strains showed a similar stimulatory response to NPY (0.1, 0.5 nmoles) on the intake of the high-fat or the low-fat diet, but the magnitude of the response was attenuated in S5B/Pl rats. In contrast, the anorectic effects of CRH (0.26 nmoles) on food deprived animals was similar in both strains for both diets. We speculate that the regulatory system controlling the intake of fat activated by galanin and β-casomorphin_(1–7) may be defective in S5B/Pl rats.