The effect of dietary fat saturation on plasma and hepatic lipoproteins in the rat

Semipurified diets containing 10% kilocalories from either safflower oil (SO), corn oil (CO), olive oil (OO) or palm oil (PO) were fed to weanling male rats for 2 weeks. The effects of dietary fat saturation on plasma lipids and lipoproteins were: 1) Nonfasted plasma cholesterol concentration was higher in rats fed OO (mean +/- SEM = 81.0 +/- 2.9 mg/dl) vs. CO (67.5 +/- 2.9); 2) plasma chylomicron cholesterol concentration was higher in rats fed OO vs. SO and CO, with PO values in between; and 3) the cholesterol concentration of plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) did not differ among groups. The effects of dietary fat saturation on hepatic lipoproteins (determined by liver perfusion techniques) were: 1) hepatic higher density lipoprotein (d = 1.006-1.21 g/ml) cholesterol production was greater in rats fed SO and CO vs. PO [19.1 +/- 1.2, 17.2 +/- 0.8 and 13.7 +/- 1.6 micrograms/(g liver X 1.5 hour), respectively]; 2) there was no difference in hepatic VLDL cholesterol production among groups; and 3) the ratio of cholesterol to protein of hepatic VLDL and the higher density lipoprotein fraction was higher in rats fed diets rich in polyunsaturated fatty acids versus saturated fatty acids. Dietary fat saturation had no effect on carcass and liver cholesterol concentrations. Since differences in hepatic lipoprotein production were not reflected in plasma lipoprotein patterns, these results suggest that extrahepatic lipoprotein metabolism differs in rats fed diets containing fatty acids of varying saturation.     

Dietary fat saturation affects apolipoprotein AII levels and HDL composition in postmenopausal women.

Increased HDL-cholesterol levels have been associated with lower coronary heart disease (CHD) risk. However, HDL are heterogeneous lipoproteins, and particles enriched in apolipoprotein (Apo) AII have been associated with increased CHD risk. We examined the effect of dietary intervention on HDL composition in 14 postmenopausal women subjected to two consecutive diet periods, i.e., an oleic acid sunflower oil diet followed by a palmolein diet, each lasting 4 wk. The linoleic acid was kept at 4% total energy and the cholesterol intake at 400 mg/d. The palmolein diet increased serum total cholesterol (TC) (P < 0.001), phospholipids (P < 0.001), Apo AII (P < 0.001), HDL cholesterol (P < 0.05), HDL lipids (P < 0.05), HDL proteins (P < 0.01) and the HDL total mass (P < 0.05). The HDL cholesterol/Apo AI ratio was increased 22.0% (P < 0.05), whereas the HDL cholesterol/Apo AII and the Apo AI/Apo AII ratios were decreased 19.4% (P < 0.01) and 30.4%, (P < 0.001), respectively. When the effects of the dietary intervention were examined according to the cholesterolemia status (< or >6.2 mmol/L), the most significant changes (P < 0.001) were related to Apo AII levels. Moreover, a significant dietary oil by cholesterol level interaction was found for Apo AII and the HDL cholesterol/Apo AII ratio. In summary, a palmolein diet increased TC and HDL cholesterol compared with oleic acid sunflower oil diet; however, the increase in Apo AII but not in Apo AI suggests the impairment of reverse cholesterol transport and potentially an increase in CHD risk. This effect was more marked in women with serum TC > 6.2 mmol/L.     

Modulation of the exercise and retirement effects by dietary fat intake in hamsters

An experiment was conducted to determine the effects and interactions of exercise-retirement and dietary fat intake on body composition and hepatic lipogenic enzyme activities in hamsters. Forty-eight adult female hamsters were randomly allotted to eight groups of six each for a 40-d experiment. Exercise was in the form of voluntary wheel-running. Four groups served as either exercise or sedentary controls and were fed either a low or a high fat diet for 40 d, in a factorial fashion. Another four groups had access to exercise for 32 d and were then retired for 8 d. Of these four groups, two were fed either the low or high fat diet for the entire 40-d period; the other two were changed to the other diet on d 32. Results showed that compared to sedentary hamsters, exercise hamsters had greater body weight gain but less body fat content and hepatic lipogenic enzyme activities. Under both sedentary and exercise conditions, high fat-fed hamsters had lower hepatic lipogenic enzyme activities and less body fat content than low fat-fed hamsters. Upon retirement, high fat feeding led to a faster increase in body fat especially in previously high fat-fed hamsters. Results of this study suggest that dietary fat intake can significantly modulate the exercise and retirement effects with respect to body weight gain and body fat content.     

Dietary fat saturation affects hepatocyte insulin binding and glucose metabolism in BHE rats

The influence of feeding 6% hydrogenated coconut oil, corn oil or menhaden oil on hepatocyte insulin binding, receptor number and glucose use was studied. Hepatocytes isolated from rats fed menhaden oil had a significantly greater affinity for insulin than hepatocytes from rats fed hydrogenated coconut oil. Glucose use was not influenced by diet; uniformly labeled glucose was metabolized to CO2 or to lipid similarly in cells isolated from rats fed the three oils. Thus, dietary fat type in a low fat diet influenced events at the plasma membrane without influencing intracellular events.     

Serum aminopeptidase A activity of mice is related to dietary fat saturation

A high intake of monounsaturated fat has been proposed to be a dietary factor that can decrease the incidence of cardiovascular disease and hypertension. In addition, increasing dietary fat saturation has been shown to increase plasma total cholesterol and elevate systolic and diastolic blood pressures. We demonstrated previously that cholesterol selectively increases in vitro aminopeptidase A activity, which is related to angiotensin metabolism. In this study, we investigated the effect of different degrees of dietary fatty acid saturation on serum aminopeptidase activities in vivo. Serum total cholesterol concentrations were also measured. Five groups of male Balb/C mice were fed for 10 wk diets containing 2.4 g/100 g of sunflower oil, fish oil, olive oil, lard or coconut oil. We measured alanyl-, arginyl-, cystinyl-, pyroglutamyl-, aspartyl- and glutamyl-specific aminopeptidase activities using arylamides as substrates. Serum total cholesterol levels were higher in mice fed diets containing saturated oils (lard and coconut) than in those consuming sunflower oil, which is unsaturated. Two of the serum aminopeptidase A activities (aspartyl and glutamyl aminopeptidase) increased progressively with the degree of saturation of the dietary fatty acids; activities were significantly greater in mice fed coconut oil than in those fed sunflower or fish oil. Therefore, the substrates hydrolyzed by this activity as well as their functions may be similarly affected. These results may have some implication for the treatment of cardiovascular disease.     

Influence of caloric contribution and saturation of dietary fat on plasma lipids in premenopausal women

Total cholesterol, HDL cholesterol, and triglycerides were measured in 31 premenopausal women randomized into one of two diet groups: one diet with a P:S ratio of 1.0 and one diet with a P:S ratio of 0.3. Both groups were fed a high-fat diet (40% of energy from fat) for four menstrual cycles per subject followed by a similar interval on a low-fat diet (20% of energy from fat). Changing from the high-fat to the low-fat diet resulted in a nonsignificant mean decrease of 7% in total cholesterol. HDL-cholesterol response to the low-fat regimen was influenced by the P:S ratio. Women in the high P:S group showed no change; mean HDL cholesterol in women in the low P:S group decreased 12%. Plasma triglycerides increased in both groups on the low-fat diet although the increase was greatest in the low P:S group.     

High fat feeding increases brown fat GDP binding in lean but not obese Zucker rats

The effects of high fat feeding on brown fat thermogenesis in rodents are controversial. In this study, we examined the effects of 8 d of high fat feeding on brown fat mitochondrial GDP binding (an in vitro index of thermogenic activity) in lean (Fa/?) and obese (fa/fa) Zucker rats. Six-week-old female rats were fed a defined low fat control diet (9.5% of energy from fat) only during the dark cycle (1200-2400 h), and food intake was measured daily at 1200, 1600, 2300, and 2400 h for 7 d (the control period). For the next 8 d, half of the lean and obese rats were fed a high fat diet (65% of energy from fat), and the others remained on the low fat control diet. Each rat was fed the amount of energy equivalent to its average energy intake during the 7-d control period. Rats were killed at 0800-1000 h. In the lean rats, high fat feeding increased GDP binding. This increased binding in the lean rats appeared to reflect levels of dietary fat and carbohydrate and was independent of caloric intake. The blunted GDP binding of the obese rats failed to respond to dietary changes.     

Consumption of high-oleic acid ground beef increases HDL-cholesterol concentration but both high- and low-oleic acid ground beef decrease HDL particle diameter in normocholesterolemic men

On the basis of previous results from this laboratory, this study tested the hypothesis that ground beef high in MUFA and low in SFA would increase the HDL-cholesterol (HDL-C) concentration and LDL particle diameter. In a crossover dietary intervention, 27 free-living normocholesterolemic men completed treatments in which five 114-g ground beef patties/wk were consumed for 5 wk with an intervening 4-wk washout period. Patties contained 24% total fat with a MUFA:SFA ratio of either 0.71 (low MUFA, from pasture-fed cattle) or 1.10 (high MUFA, from grain-fed cattle). High-MUFA ground beef provided 3.21 g more 18:1(n-9), 1.26 g less 18:0, 0.89 g less 16:0, and 0.36 g less 18:1(trans) fatty acids per patty than did the low-MUFA ground beef. Both ground beef interventions decreased plasma insulin and HDL(2) and HDL(3) particle diameters and increased plasma 18:0 and 20:4(n-6) (all P ≤ 0.05) relative to baseline values. Only the high-MUFA ground beef intervention increased the HDL-C concentration from baseline (P = 0.02). The plasma TG concentration was positively correlated with the plasma insulin concentration (r = 0.40; P < 0.001) and negatively correlated with HDL-C (r = -0.47; P < 0.001) and plasma 18:0 (r = -0.24; P < 0.01). Plasma insulin and HDL diameters were not correlated (r = 0.01; P > 0.50), indicating that reductions in these measures were not coordinately regulated. The data indicate that dietary beef interventions have effects on risk factors for cardiovascular disease that are independent (insulin, HDL diameters) and dependent (HDL-C) on beef fatty acid composition.     

Effect of dietary fat on opiate receptor binding and body composition in mice

C57BL/6 and C3H male mice were fed either a 25% corn oil, 25% butter fat, or chow diet ad libitum for 6 weeks. At that time, opiate receptor binding in the brain and body composition was determined. Regardless of the type of dietary fat, both groups fed with high-fat diets in each strain of mice exhibited obesity in the absence of hyperphagia as compared with their chow-fed counter-parts. Scatchard analysis of opiate receptor binding from the brains of C57BL/6 mice fed with the polyunsaturated fat diet (corn oil) demonstrated a decreased K_D relative to the saturated fat-fed group with no significant difference in B_max. The C3H mice exhibited no significant differences in either binding affinity or receptor number within the three dietary groups. Fatty acid analysis of the synaptic plasma membrane showed changes in the C18:1 ω-9, C18:2 ω-6, and C22:6 ω-3 fatty acid composition. C18:1 ω-9 was elevated while C22:6 ω-3 was depressed in corn oil compared to butter fat-fed C57BL/6 mice. There were no differences in membrane fluidity as measured by fluorescence polarization.     

Fetal programming of dietary fructose and saturated fat on hepatic quercetin glucuronidation in rats

ObjectivePhase II biotransformation of flavonoids generates bioactive metabolites in vivo. However, data on the effect of environmental and physiologic factors and fetal programming on phase II pathways toward flavonoids are limited. We examined the effect of parental exposure to a diet high in saturated fats and fructose 1 mo before conception through lactation on in vitro hepatic uridine 5′-diphosphate (UDP)-glucuronosyltransferase (UGT) activity toward quercetin in parent and offspring rats and the interaction between diet and sex.MethodsParents were fed a diet containing 9.9% coconut fat, 0.5% cholesterol, 30% fructose, and 30% glucose (SFF) or a control (C) diet containing 11% corn oil and 60% glucose. After weaning, offspring were fed the C diet for an additional 12 wk. The glucuronidation rate of microsomal UGT was determined with quercetin 30 μmol/L and 12.5 μg of protein in a total volume of 100 μL after a 15-min incubation at 37°C. Three quercetin glucuronides (7-O-quercetin glucuronide, 4′-O-quercetin glucuronide, and 3′-O-quercetin glucuronide) were quantified.ResultsIn the parent females, the SFF diet decreased by 29% and 19% the production rate of 3′- and 4′-O-quercetin glucuronide quercetin glucuronides, respectively, compared with the C diet (P ≤ 0.05). The production rate of 7-O-quercetin glucuronide quercetin glucuronide in the female offspring rats born to C dams was 59% larger than in their male counterparts (P < 0.05), but no difference was observed in the offspring of SFF dams.ConclusionHigh dietary fructose and saturated fat decreased UGT capacity toward quercetin in female rats and in utero exposure to the diet decreased the glucuronidation capacity of their pups.     

High dietary fat intake increases renal cyst disease progression in Han:SPRD-cy rats

The effect of a high level of dietary fat on renal cyst disease was examined in the Han:SPRD-cy rat model of polycystic kidney disease. Control and diseased rats at 4 wk of age were fed either a low fat or high fat diet (5 or 20 g/100 g diet) for 6 wk. In rats with kidney disease fed the high fat rather than the low fat diet, kidneys were 17% larger, renal fluid content was 19% higher and cyst scores were 30% higher, indicating greater disease progression. In diseased rats fed the high fat diet, serum urea was 25% higher, indicating worsened renal function. Serum creatinine was 49% higher only in males. To examine whether high dietary fat worsened renal cyst disease by altering sex hormone concentrations, serum testosterone and estrogen concentrations were determined. In normal compared with diseased male rats, serum testosterone concentrations were one to three times higher. Serum testosterone concentrations were higher in normal male rats fed the high compared with the low fat diet, but were not affected by diet in diseased rats. Serum estrogen concentrations were unaffected by dietary fat levels or by disease state. Although it remains to be elucidated how dietary fat influences sex hormone concentrations in this disease, the current study demonstrates that a high dietary fat intake increases kidney disease progression in Han:SPRD-cy rats.     

High fat intake lowers hepatic fatty acid synthesis and raises fatty acid oxidation in aerobic muscle in Shetland ponies.

The metabolic effects of feeding soyabean oil instead of an isoenergetic amount of maize starch plus glucose were studied in ponies. Twelve adult Shetland ponies were given a control diet (15 g fat/kg DM) or a high-fat diet (118 g fat/kg DM) according to a parallel design. The diets were fed for 45 d. Plasma triacylglycerol (TAG) concentrations decreased by 55 % following fat supplementation. Fat feeding also reduced glycogen concentrations significantly by up to 65 % in masseter, gluteus and semitendinosus muscles (P < 0.05 and P < 0.01 and P < 0.01 respectively). The high-fat diet significantly increased the TAG content of semitendinosus muscle by 80 % (P < 0.05). Hepatic acetyl-CoA carboxylase and fatty acid synthase activities were 53 % (P < 0.01) and 56 % (P < 0.01) lower respectively in the high-fat group, but diacylglycerol acyltransferase activity was unaffected. Although carnitine palmitoyltransferase-I (CPT-I) activity in liver mitochondria was not influenced, fat supplementation did render CPT-I less sensitive to inhibition by malonyl-CoA. There was no significant effect of diet on the activity of phosphofructokinase in the different muscles. The activity of citrate synthase was raised significantly (by 25 %; P < 0.05) in the masseter muscle of fat-fed ponies, as was CPT-I activity (by 46 %; P < 0.01). We conclude that fat feeding enhances both the transport of fatty acids through the mitochondrial inner membrane and the oxidative capacity of highly-aerobic muscles. The higher oxidative ability together with the depressed rate of de novo fatty acid synthesis in liver may contribute to the dietary fat-induced decrease in plasma TAG concentrations in equines.     

Interaction between dietary fat intake and the cholesterol ester transfer protein TaqIB polymorphism in relation to HDL-cholesterol concentrations among US diabetic men

BACKGROUND: A low plasma HDL-cholesterol concentration is a major characteristic of diabetic dyslipidemia. HDL concentrations are determined by both environmental factors and genetic factors. Cholesterol ester transfer protein (CETP) plays an important role in the regulation of HDL metabolism, and the TaqIB polymorphism of the CETP gene has been associated with elevated HDL concentrations. OBJECTIVE: We examined the association between the CETP TaqIB polymorphism and plasma HDL concentrations and evaluated whether this association was modified by dietary fat intake. DESIGN: We followed 780 diabetic men aged 40-75 y who participated in the Health Professionals Follow-Up Study since its initiation in 1986. The participants had confirmed type 2 diabetes and were free of cardiovascular disease at the time blood was drawn. RESULTS: After adjustment for age, smoking, alcohol consumption, fasting status, hemoglobin A(1c), physical activity, total energy intake, and body mass index, HDL concentrations were significantly higher in men with the B2B2 or B1B2 genotype than in those with the B1B1 genotype (adjusted x +/- SE: 37.9 +/- 0.02, 40.3 +/- 0.01, and 42.6 +/- 0.02 mg/dL for B1B1, B1B2, and B2B2, respectively; P for trend = 0.0004). This inverse association of the B1 allele with plasma HDL concentrations existed for those with a high consumption of animal fat (P for interaction = 0.02), saturated fat (P for interaction = 0.02), and monounsaturated fat (P for interaction = 0.04). CONCLUSION: These data confirmed a significant effect of the CETP Taq1 gene on HDL concentrations and suggested a potential interaction between the CETP TaqIB polymorphism and intake of dietary fat on plasma HDL concentration.     

Changes in dietary lipid saturation modify fatty acid composition and high-density-lipoprotein binding of adipocyte plasma membrane

Binding of rat high-density lipoprotein (HDL) to adipocyte plasma membranes appears to be mediated by specific protein-recognition sites, but membrane lipids may also affect these interactions. To study the effect of dietary fatty acid composition on adipocyte-membrane phospholipid composition and HDL binding, male Wistar rats (250 +/- 10 g) were fed diets high in polyunsaturated (20% wt:wt sunflowerseed oil) or saturated and monounsaturated fatty acids (20% lard, by weight). Sunflower-oil vs lard feeding significantly increased the polyunsaturated fatty acid content of membrane diacylglycerophospholipids and the (22:0 and 24:0) content of long-chain fatty acids of sphingomyelin (p less than 0.05) from epididymal and perirenal adipocyte plasma membranes. Concomitant with these changes in membrane phospholipid composition, sunflower-oil vs lard treatment significantly increased the maximum binding capacity (Bmax) of 125I-labeled HDL2 (p less than 0.05). These results show that feeding polyunsaturated fatty acids enhanced HDL2 Bmax of adipocyte plasma membranes, possibly as a consequence of altering the fatty acid composition of membrane phospholipids.     

Molasses increases HDL cholesterol in rats research note

Two experiments were conducted to determine whether molasses might exert effects on serum lipoproteins. In experiment 1, 24 rats were divided into two groups and fed diets containing liquid molasses from sugar beet or sucrose (7.71 g of molasses dry matter or sucrose per kg of diet). The second experiment included four groups of rats (n = l2/group) and was conducted in a bifactorial design, with the factors being molasses (non-supplementation vs. supplementation of 77.1 g of molasses dry matter per kg of diet at the expense of sucrose) and dietary cholesterol (0 vs. 5 g/kg diet). In experiment 1, the ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL) cholesterol concentration tended to be lower in rats fed the molasses diet than in rats fed the control diet (p < 0.15). In experiment 2, rats fed the molasses diet had higher concentrations of HDL cholesterol (+ 26%) than control rats fed diets without molasses (p < 0.05). This effect was independent of the dietary cholesterol concentration. Concentrations of cholesterol in LDL, very low-density lipoprotein (VLDL), and liver as well as concentrations of triacylglycerols in plasma and liver remained unaffected by molasses in both experiments. In conclusion, the results of this study suggest that supplementation of molasses is effective at raising HDL cholesterol levels in rats.     

Dietary fat saturation distinctly affects apolipoprotein gene expression and high density lipoprotein size distribution in two strains of Golden Syrian hamsters

Plasma lipoprotein levels, high density lipoprotein (HDL) particle size distribution and tissue mRNA levels for several apolipoproteins were determined in two strains of Golden Syrian hamsters characterized as high (F1B) or low (LVG) responders to atherogenic diets. Twenty-four male hamsters per strain were fed semipurified diets containing 0.2 g/100 g diet cholesterol and 15 g/100 g diet fat enriched (13 g/100 g) with either coconut oil or soybean oil for 18 weeks. HDL size was analyzed by non-denaturing gradient (4–30%) polyacrylamide gel electrophoresis, and categorized into four HDL subspecies according to Stoke’s diameter. Hepatic and intestinal mRNA apolipoprotein concentrations were measured using solution hybridization/ribonuclease protection assay. Compared to F1B hamsters, the LVG hamsters showed a less atherogenic lipoprotein profile; with lower triglycerides (P < 0.01) and higher HDL cholesterol (P < 0.01) levels. Consumption of a polyunsaturated fatty acid (PUFA) diet induced the decrease in triglyceride levels (42% in LVG, P < 0.05 and 51% in F1B, P < 0.01) and in HDL cholesterol (15% in LVG, P < 0.05 and 28% in F1B, P < 0.01). LVG animals had a greater proportion of larger HDL particles than F1B animals regardless of the diet (P < 0.01). Consumption of the soybean oil diet, compared with coconut oil diet, lowered the proportion of HDL2b and increased the proportion of HDL2a and HDL3 in LVG animals. However, F1B animals consuming the PUFA diet had a decrease in the percentage of HDL2b and HDL2a and a marked increase in HDL3. ApoA-I mRNA levels were higher in F1B animals (P < 0.01), and were not affected by dietary fat saturation in either strain of hamsters. ApoA-II mRNA levels were higher in the LVG strain (P < 0.001), and increased with fat saturation of both strains (P < 0.05). The average ratio of intestinal apoC-II/C-III mRNA was 3.2 times higher in LVG animals (P < 0.05) as compared with F1B animals. This is consistent with a higher lipolytic activity in LVG animals that will result in lower triglyceride concentrations and increased HDL particle size. Dietary induced effects on HDL particle size may be attributed to the higher levels of apoA-II mRNA as well as an increased neutral lipid exchange between HDL and triglyceride-rich lipoproteins due to the elevated triglyceride levels in animals fed on saturated diet.     

Serum gastrin increases with increasing dietary calcium but not with increasing dietary fat or fiber in Fischer-344 rats.

We studied the effects of dietary calcium, fat and fiber on serum gastrin in Fischer-344 rats in a full factorial experiment as part of a larger study of diet and colon cancer risk factors. Nine- to 10-wk-old male rats were fed standard or experimental diets for 4 wk. Wheat bran was the sole source of fiber. Wheat bran levels were 0, 2.5, 10 and 20%; fat levels were 1, 5 and 10%; calcium levels were 0.18, 0.52 and 1.04% of diet weight. On d 29 serum was collected and stored at -80 degrees C until analyzed. There was a significant (P less than 0.0001) dose-dependent increase in serum gastrin from 102 to 173 ng/L, with increasing calcium. No other significant changes in serum gastrin were noted with the dietary changes. A long-term change in the level of serum gastrin, caused by dietary modification, will influence the trophic effect that gastrin has on colonic mucosa as well as on colon carcinomas. We speculate that calcium supplementation, although slowing colonic proliferation, might have an undesirable effect on the growth of early undetected colonic tumors.     

Impact of dietary protein on lipid metabolism in hamsters is source-dependent and associated with changes in hepatic gene expression

This study tested the hypothesis that protein source is a factor determining the impact of the diet on lipid metabolism in hamsters. Twenty-eight hamsters of similar body weight were assigned for a period of 8 weeks to one of the following four diets (seven per group) containing either 20 % (w/w) casein (CAS), beef protein (BF), wheat gluten (WG) or soya protein (SOY). The fat composition of the diet was the same (15.5 % w/w) in all groups and provided SFA, MUFA and PUFA representative of the average Canadian diet. After an overnight fast, blood and liver were collected for the measurement of serum lipids, fatty acid composition of liver phospholipids and mRNA levels of selected genes involved in lipid metabolism. WG resulted in lower total cholesterol, HDL-cholesterol and non-HDL-cholesterol but, along with SOY, in higher mRNA levels of cholesterol 7 alpha-hydroxylase and LDL receptor. Furthermore, both WG and SOY resulted in lower 18 : 3n-3, 20 : 4n-6, total n-6 PUFA, 18 : 1n-9 and total MUFA, but higher 22 : 6n-3, total n-3 PUFA, 22 : 6n-3/18 : 3n-3 and 22 : 5n-3/18 : 3n-3 ratios in liver phospholipids, and higher hepatic Delta6-desaturase mRNA levels. These results show that the impact of dietary protein on lipid metabolism is source-dependent and associated with changes in mRNA abundances of key hepatic enzymes and receptors.