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.     

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.     

Extracellular Hypothalamic Monoamines Measured by In Vivo Microdialysis in a Rat Model of Dietary Fat-Induced Obesity

We tested two hypotheses about monoamine neurotransmitters in two strains of rats that differ in their sensitivity to obesity when eating a high-fat diet; 1) that the concentrations of norepinephrine and serotonin and of their metabolites differ in the extracellular fluid of tlie ventromedial hypothalamus of conscious, unrestrained Osborne-Mendel and S 5B/PI rats, and 2) that these monoamines are altered differently between strains by a high-fat diet. The monoamines were measured by HPLC in dialysate collected by in vivo microdialysis in rats eating a semisyntlietic low-fat diet (10% of kcal as fat) and again after either two or seven days of eating a high-fat diet (56 % of kcal as fat). Norepinephrine, serotonin (5-HT), and 5-hydroxyindole-3-acetic acid (5-HIAA) were lower in Osborne-Mendel rats than in S 5BR1 rats eating the low-fat diet. Norepinephrine and serotonin both increased in Osborne-Mendel rats with the onset of tlie high-fat diet so that Osborne-Mendel and S 5B/PI rats no longer differed in these neurotransmitters. By day 7 of high-fat feeding, the concentrations of 3-methoxy-4-hydroxyplienylglycol (MHPG), 5-HIAA and the 5-HIAA/5-HT ratio rose in both strains. Ambient extracellular monoamines in the medial hypothalamus are lower in Osborne-Mendel rats than in S 5B/PI rats and the response of these catecholamines to dietary fat was greater in Osborne-Mendel rats than in S 5B/PI rats.     

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.     

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.     

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.     

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.     

Differential Metabolic Effects of Energy Restriction in Dogs Using Diets Varying in Fat and Fiber Content

The role of dietary fat and fiber in energy restriction for the management of obesity was examined. Twelve male castrated dogs were energy restricted for 7 weeks by feeding 60% of their calculated maintenance energy requirements (MER = 1500 kcal/m²/d) for ideal body weight. Six dogs were restricted on a high-fat (35.4 kcal% from fat), low-fiber (2.9% dry matter basis [DMB]) diet while the other six dogs were restricted on a low-fat (24.5 kcal% from fat), high-fiber (27% DMB) diet. Compared with the high-fat, low-fiber diet, energy restriction on the low-fat, high-fiber diet resulted in significantly greater decreases in body fat (1472 ± 166 vs. 853 ± 176 g; p < 0.05) and total serum cholesterol concentrations (108.7 ± 11.3 vs. 51.5 ± 13.9 mg/dL; p< 0.005). Reductions in body weight (2.86 ± 0.3 vs. 2.14 ± 0.3 kg; p< 0.09), and mean arterial blood pressure (17.4 ± 6.1 vs. 6.7 ± 2.9 mmHg; p < 0.12) were also greater on the low-fat diet; however, these diet effects did not reach statistical significance. These data suggest that the fat and fiber content of the diet during energy restriction are important factors in the management of obesity.     

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.     

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.     

The effect of an acute fat load on endothelial function after different dietary regimens in young healthy volunteers

Attention has recently been focused on endothelial function after a single high-fat meal, i.e. on the anticipated direct atherogenic effect of triglyceride-rich lipoproteins. Our study was designed to investigate the effect of a low-fat diet given for four weeks followed by a high-fat diet for another four weeks. At the end of each dietary period, a noninvasive ultrasound investigation of endothelial function of the brachial artery was performed along with laboratory tests. Endothelial function was measured immediately before the dietary load and after three and six hours in 11 healthy volunteers. The results were expressed as percentage of the changes in artery diameter at rest and during hyperemia; the data were processed using computer technology. When compared to the low-fat regimen, the total cholesterol content rose after the high-fat diet from 4.28 mmol/l to 5.15 mmol/l (p<0.05) in the whole group of volunteers. There was no difference between both dietary regimens in baseline triglycerides. The brachial artery dilatation under basal conditions was 5.26+/-2.88 mm after the high-fat diet compared with the value of 3.13+/-3.01 mm (p<0.05) after the low-fat diet. When measured individually endothelial function in the whole group of volunteers in the course of the day, the degree of arterial dilatation after one month on low-fat diet was 3.13+/-3.0%, 3.88+/-2.5% and 5.23+/-3.3% at single measurement. When comparing arterial dilatation at two closest measurements, a non-significant trend, p>0.05 was seen in either case. The following values were obtained after one month on the high-fat diet: 5.26+/-2.9%, 4.47+/-1.7%, and 6.2+/-3.6%; again showing a non-significant trend of p>0.05. In this study, a single high-fat meal at the different dietary regimen did not significantly influence the vasoreactivity of the brachial artery in young volunteers.     

Effects of a High-Fat Diet and Strain on Hypothalamic Gene Expression in Rats

Objective: This study was designed to investigate whether dietary fat and genetic background might differentially alter the expression of hypothalamic genes involved in food intake. Research Methods and Procedures: Three-month-old Osborne-Mendel (OM) and S5B/Pl rats were fed either a high-fat or a low-fat diet for 14 days. mRNA for neuropeptide Y (NPY), corticotrophin-releasing hormone, NPY Y-1 receptor and Y-5 receptor, and serotonin 2c (5-HT2c) receptors were measured using Northern blotting or ribonuclease protection assays. Results: OM rats showed an increased expression of NPY and corticotrophin-releasing hormone compared with S5B/Pl rats. The expression of NPY-Y1 and -Y5 receptor mRNA was significantly higher in the hypothalamus of OM rats compared with S5B/Pl rats. The expression of 5HT-2c receptor mRNA was significantly reduced in both strains of rats eating a high-fat diet when compared with the animals eating the low-fat diet. Discussion: These data suggest that over activity of the NPY system may contribute to the development of obesity in OM rats and that expression of the 5HT-2c receptor gene may be modulated by dietary fat.     

Effect of a selective OX1R antagonist on food intake and body weight in two strains of rats that differ in susceptibility to dietary-induced obesity

An orexin-1 receptor antagonist decreases food intake whereas orexin-A selectively induces hyperphagia to a high-fat diet. In the present study, we evaluated the effect of an orexin antagonist in two strains of rats that differ in their sensitivity to becoming obese while eating a high-fat diet. Male Osborne-Mendel (OM) and S5B/Pl (S5B) rats were treated acutely with an orexin-1 receptor antagonist (SB-334867), after adaptation to either a high-fat (56% fat energy) diet or a low-fat (10% fat energy) diet that were equicaloric for protein (24% energy). Ad libitum fed rats were injected intraperitoneally with SB-334867 at doses of 3, 10 or 30 mg/kg, or vehicle at the beginning of the dark cycle, and food intake and body weight were measured. Hypothalamic prepro-orexin and orexin-1 receptor mRNA expression were analyzed in OM and S5B rats fed at a high-fat or low-fat diet for two weeks. SB-334867 significantly decreased food intake in both strains of rats eating the high-fat diet but only in the OM rats eating the low fat diet. The effect was greatest at 12 and 24 h. Body weight was also reduced in OM rats 1d after injection of SB-334867 but not in the S5B rats. Prepro-orexin and orexin-1 receptor expression levels did not differ between strains or diets. These experiments demonstrate that an orexin antagonist (SB-334867) reduces food intake and has a greater effect in a rat strain that is susceptible to dietary-induced obesity, than in a resistant strain.     

Renal infarction due to polyarteritis nodosa in a patient with angioimmunoblastic T-cell lymphoma: a case report and a brief review of the literature

ABSTRACT: Angioimmunoblastic T-cell lymphoma (AITL) is one of the most common subtypes of peripheral T-cell lymphoma (15-20% of all cases), accounting for approximately 1-2% of all non-Hodgkin lymphomas. It often presents autoimmune phenomena including hemolytic anemia, thrombocytopenia, glomerulonephrities and circulating immune complexes (CIC). Polyarteritis nodosa (PAN) is an autoimmune disease characterized by necrotizing vasculitis of medium vessels, which rarely develops in association with hematological malignant disorders. Herein we report the case of a male patient with AITL who had a renal infarction secondary to PAN, mimicking a neoplastic lesion. A 40-year-old man underwent lymph node biopsy in the suspicious of sarcoidosis. On the basis of histological and immunohistochemical findings, a diagnosis of AITL was performed. The patient was successfully treated with a cytarabine-based regimen for 6 cycles. Three months after the initial diagnosis of AITL, a whole body CT-scan showed a lesion in the lower pole of the left kidney. A renal cell carcinoma was suspected, thus a nephrectomy was carried out. The histological findings were compatible with polyarteritis nodosa. To the best of our knowledge, the association between PAN and AITL has been described only once. This relation may be secondary to the induction of an autoimmune phenomenon by the lymphoma with the formation of circulating immune complexes, leading to vessel walls injury. A careful evaluation is needed in the management of AITL patients with signs of renal failure in order to avoid delay of treatment and organ damage. Key words: renal infarction, polyarteritis nodosa, T-cell lymphoma.     

Feeding Response of Rats to No-Fat and High-Fat Cakes

The nutritional effects of high-fat diets have been extensively studied in laboratory animals, but as yet few experiments have examined the feeding response of animals to newly developed fat substitutes. The present study used commercially available no-fat (0% fat, 92% carbohydrate) and high-fat (41% fat, 54% carbohydrate) cake to determine the effects of fat substitutes on food preference and caloric intake in rats. The first experiment showed that nondeprived rats found the high-fat and no-fat cakes equally palatable and highly preferred to lab chow. Food deprived rats, however, preferred the high-fat cake to the no-fat cake, which may be related to its higher caloric density. In the second experiment, rats fed high-fat cake, in addition to chow, for 30 days consumed more calories and gained more weight than did rats fed no-fat cake and chow. The no-fat cake group, however, overate and gained more weight than chow-only controls. The hyperphagic response to the no-fat cake can be attributed to its carbohydrate content, moisture, and high palatability. Thus, removing fat from the cake reduced, but did not eliminate, its obesity-promoting effect. Obviously, low-fat foods must be consumed in moderation if used for weight control.     

Development of hepatic and adipose tissue lipogenic enzymes and insulinemia during suckling and weaning on to a high-fat diet in Zucker rats

This study was designed to monitor the developmental changes in insulinemia and lipogenic enzyme activities in both inguinal adipose tissue and liver during suckling (7, 9, 14, and 17 days of age) and weaning (22 and 30 days of age) on to either a low-fat or a high-fat diet in lean (Fa/fa) and obese (fa/fa) rats. Tissues were removed through surgery and genotypes were retrospectively determined. During suckling, there was no difference in liver enzyme activities between the two groups. In contrast, adipose tissue fatty acid synthetase was increased by 50% and citrate cleavage enzyme and malic enzyme by 30% by 9 days of age. By 17 days of age, there was a threefold elevation in these enzyme activities and 6-phosphogluconic dehydrogenase and a twofold increase in glucose-6-phosphate dehydrogenase per inguinal fat pad in fa/fa versus Fa/fa. Consistent with these results, fat pad weight was increased by 20%, 50%, and 100% at 9, 14, and 17 days of age, respectively, in obese as compared to lean pups. However only by 17 days of age could a slight but significant increase in insulin level be detected in obese pups. Enlargement of inguinal fat pad accelerated after weaning on to a low-fat diet and still more after weaning on to a high-fat diet. Weaning on to a low-fat diet elicited an induction of hepatic lipogenic enzymes two or three times greater in fa/fa than in lean pups, while weaning on to a high-fat diet blunted the differences between genotypes. The lipogenic enzyme activities displayed per total inguinal fat were three to ten times greater in obese than in lean pups, regardless of the diet. However, adipose tissue lipogenic enzyme activities were much lower after weaning on to a high-fat than on to a low-fat diet in obese pups. The high-fat diet was as effective as the low-fat diet in triggering hyperinsulinemia in obese pups. The increased adipose tissue capacity for lipogenesis, starting during the suckling period, could play an important etiologic role in the development and maintenance of obesity in the Zucker rat.-Bazin, R., and M. Lavau. Development of hepatic and adipose tissue lipogenic enzymes and insulinemia during suckling and weaning on to a high-fat diet in Zucker rats.     

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.     

Hypertension,Thrombosis, and Atherosclerosis in the Rat

A simple high fat diet containing cholic acid has been devised for producing hyperlipemia and an increased incidence of thrombosis in the small coronary vessels of the rat, but without producing significant atherosclerotic lesions. The influence on this syndrome induced by six weeks of desoxycorticosterone administration, 2 mg. daily, and 10 weeks of oral saline (1%) ingestion was investigated in 30 115-g. male rats. Marked hypertension developed only when it was induced prior to beginning the dietary feeding. In comparison to the control groups, the group that was both hyperlipemic and hypertensive had severer hypertension, severer hyperlipemia, double the mortality due to thrombosis and fatty streaks in the aorta but very few lesions of periarteritis nodosa. However, the early atherosclerotic lesions did not seem to be responsible for the increased production of thrombosis. It is therefore probable that under these experimental conditions hypertension has a more direct action on the production of thrombotic effect than that of worsening the atherosclerotic lesions.     

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.     

Weight regain after sustained weight reduction is accompanied by suppressed oxidation of dietary fat and adipocyte hyperplasia

A dual-tracer approach (dietary 14C-palmitate and intraperitoneal 3H-H2O) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were allowed to mature under obesogenic conditions for 16 wk. One group was switched to ad libitum feeding of a low-fat diet for 10 wk (Obese group). The remaining rats were switched to an energy-restricted, low-fat diet for 10 wk that reduced body weight by 14% and were then assessed in energy balance (Reduced group), with free access to the low-fat diet (Relapse-Day1 group), or with a provision that induced a minor imbalance (+10 kcal) equivalent to that observed in obese rats (Gap-Matched group). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.