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PubMed1986

Diurnal variations in the effects of an unsaturated-fat-containing diet on fatty acid and cholesterol synthesis in rat hepatocytes.

Rats were fed ad libitum on either a standard high-carbohydrate diet, or a standard diet supplemented with 15% corn oil. Hepatocytes were prepared either during the light phase (L2-hepatocytes) or during the dark phase (D6-hepatocytes) of the diurnal cycle. In hepatocytes from rats fed on the fat-containing diet, fatty acid synthesis (lipogenesis) was suppressed to a much greater extent at D6 than at L2. The magnitude of the increase in plasma-free fatty acid concentration was similar at the two times of day. The rate of cholesterol synthesis was also significantly suppressed in the D6- but not in the L2-hepatocytes. This differential inhibition resulted in the abolition of the normal diurnal rhythm of cholesterogenesis. The initial activity of 3-hydroxy-3-methylglutaryl-CoA reductase in hepatocytes was also suppressed by corn-oil feeding at D6 but not at L2. In D6-hepatocytes, the inhibitory effect of the high-fat diet on the conversion of lactate into cholesterol and fatty acids was greater than that on total carbon flux into these substances for all endogenous sources. Despite this, under these conditions a high concentration of lactate and pyruvate resulted in a several-fold stimulation of total carbon flux into fatty acids. In hepatocytes prepared at L2, fat-feeding had little effect on the degree of stimulation of lipogenesis by insulin or inhibition by glucagon. However, at D6, fat-feeding blunted the response of lipogenesis to both these hormones.

Animals↗
PubMed1976

The effect of an unsaturated-fat diet on cataract formation in streptozotocin-induced diabetic rats.

1. Cataract formation in streptozotocin-induced diabetes in rats was reduced by approximately 85% when a diet rich in maize oil (300 g/kg diet) (fat diet) was given, thus confirming results of earlier studies. However, the concentration of sorbitol in the lens of diabetic animals remained high, the values for diabetic rats given the standard diet and the fat died being 65 and 40 mumol/g protein respectively. 2. With the standard diet, the fatty acid profile of the triglycerides of the epididymal fat pads was characterized by a greater relative proportion of saturated fatty acids for the diabetic animals compared to that for the normal animals. The fat diet moderated the tendency towards saturation in the diabetic animals. 3. The fat diet had other effects on the diabetic animals; these included a reduced mortality rate, increased body-weight, a decrease in the daily water intake, and in the daily urinary excretion of glucose and urea. 4. In the diabetic animals the fat diet had no effect on the specific activities in the liver of hexokinase (EC 2.7.1.1), glucokinase (EC 2.7.1.2), phosphofructokinase (EC 2.7.1.11) and pyruvate kinase (EC 2.7.1.40). However, the specific activity of glucose-6-phosphatase (EC 3.1.3.9) was reduced, while that of malate dehydrogenase (decarboxylating) (NADP) (EC 1.1.1.40) was increased. The NAD+:NADH ratio, as calculated from liver pyruvate and lactate concentrations, tended to increase. 5. The results suggested that the fat diet moderated the long-term metabolic effects of diabetes.

Animals↗
PubMed1997

It is more important to increase the intake of unsaturated fats than to decrease the intake of saturated fats: evidence from clinical trials relating to ischemic heart disease.

The evidence from formal, controlled, long-term clinical trials that changes in dietary fats reduce the incidence of ischemic (coronary) heart disease (IHD) is unimpressive. Mostly these trials were underpowered and in several the rigor of dietary control in the intervention and control groups was inadequate. Six controlled clinical trials in healthy people of diets low in saturated fat and cholesterol, also accompanied by changes in other risk factors, were unsuccessful in reducing the incidence of IHD. An exception was the Oslo trial in which concurrent cigarette smoking was almost halved. Similarly, in the only two clinical trials of the secondary prevention of IHD through use of diets low in saturated fats and cholesterol there was no significant effect on IHD recurrence rate. This may relate to poor compliance outside strict clinic conditions. In contrast, five of six secondary prevention trials in which diets low in saturated fats were supplemented with polyunsaturated fats reduced IHD deaths and, to a lesser extent, all-cause mortality. No formal trial has been reported of the effects on IHD of diets high in monounsaturated fats. The greatest benefit for patients with IHD has come from diets supplemented with n-3 fatty acids (two trials), and this benefit was independent of changes in plasma lipoproteins. The evidence from these clinical trials indicates that more emphasis should be given in national and international dietary recommendations to supplementation with polyunsaturated fats, particularly foods rich in n-3 fatty acids, than to diets low in total and saturated fats.

Adult↗
PubMed1993

Influence of feeding unsaturated fats on growth and immune status of mice.

Dietary polyunsaturated fatty acids alter the lipid composition and immune systems of mice. To date, most studies have been of short duration and focused on a particular immunologic assay. Adult female mice were therefore fed diets rich in 18:1(n-9) (olive oil), 18:2(n-6) (safflower oil), 18:3(n-3) (linseed oil) or 20:5(n-3) and 22:6(n-3) (fish oil-safflower oil, 9:1, wt/wt), for a 5-mo period, encompassing two breeding cycles. Offspring from the second breeding cycle were then fed these diets for 42 d, and a spectrum of immune functions was assessed. Dietary fat had a small effect on gestational weight gain and total and relative organ weights of the offspring. The relative amounts of splenic Ly-2 and gamma delta receptor-expressing T cells were proportional to the concentration of 18:2(n-6), and inversely proportional to the concentration of long chain (n-3) polyenes in the diet. In contrast, Ly-1, immunoglobulin M, GM1+, and Ly-1 B suppressor inducer cells were not significantly affected by dietary fat. Splenic natural killer cell and lymphokine activated killer cell activities were attenuated by (n-3) polyunsaturated fatty acids, in contrast to superoxide production of stimulated macrophages which was increased. Those immune functions that were sensitive to dietary fat modulation will be the focus of continued research.

Animals↗
PubMed2003

A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein (a) compared with a diet rich in unsaturated fat in women.

The effects of high and low fat diets with identical polyunsaturated/saturated fatty acid (P/S) ratios on plasma postprandial levels of some hemostatic variables and on fasting lipoprotein (a) [Lp(a)] are not known. This controlled crossover study compared the effects of a high fat diet [38.4% of energy (E%) from fat; HSAFA-diet, P/S ratio 0.14], a low fat diet (19.7 E% from fat; LSAFA-diet, P/S ratio 0.17), both based on coconut oil, and a diet with a high content of monounsaturated fatty acids (MUFA) and PUFA (38.2 E% from fat; HUFA-diet, P/S ratio 1.9) on diurnal postprandial levels of some hemostatic variables (n = 11) and fasting levels of Lp(a) (n = 25). The postprandial plasma concentration of tissue plasminogen activator antigen (t-PA antigen) was decreased when the women consumed the HSAFA-diet compared with the HUFA-diet (P = 0.02). Plasma t-PA antigen was correlated with plasminogen activator inhibitor type 1 (PAI-1) activity when the participants consumed all three diets (Rs = 0.78, P < 0.01; Rs = 0.76, P < 0.01; Rs = 0.66, P = 0.03; on the HSAFA-, the LSAFA- and the HUFA-diet, respectively), although the diets did not affect the PAI-1 levels. There were no significant differences in postprandial variations in t-PA activity, factor VII coagulant activity or fibrinogen levels due to the diets. Serum fasting Lp(a) levels were lower when women consumed the HSAFA-diet (13%, P < 0.001) and tended to be lower when they consumed the LSAFA-diet (5.3%, P = 0.052) than when they consumed the HUFA-diet. Serum Lp(a) concentrations did not differ when the women consumed the HSAFA- and LSAFA-diets. In conclusion, our results indicate that a coconut oil-based diet (HSAFA-diet) lowers postprandial t-PA antigen concentration, and this may favorably affect the fibrinolytic system and the Lp(a) concentration compared with the HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy seem to have a beneficial influence on Lp(a) levels.

Adult↗
PubMed2000

Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study.

OBJECTIVES: Insulin resistance (IR) has been increasingly implicated in the pathogenesis of gout. The lipoprotein abnormalities described in hyperuricaemic subjects are similar to those associated with IR, and insulin influences renal urate excretion. In this study it was investigated whether dietary measures, reported to be beneficial in IR, have serum uric acid (SU) and lipid lowering effects in gout. METHODS: Thirteen non-diabetic men (median age 50, range 38-62) were enrolled. Each patient had had at least two gouty attacks during the four months before enrollment. Dietary recommendations consisted of calorie restriction to 6690 kJ (1600 kcal) a day with 40% derived from carbohydrate, 30% from protein, and 30% from fat; replacement of refined carbohydrates with complex ones and saturated fats with mono- and polyunsaturated ones. At onset and after 16 weeks, fasting blood samples were taken for determination of SU, serum cholesterol (C), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), and triglycerides (TGs). Results were expressed as median (SD). RESULTS: At onset, the body mass index (BMI) was 30.5 (8.1) kg/m(2). Dietary measures resulted in weight loss of 7.7 (5.4) kg (p=0.002) and a decrease in the frequency of monthly attacks from 2.1 (0.8) to 0.6 (0.7) (p=0.002). The SU decreased from 0.57 (0.10) to 0.47 (0.09) mmol/l (p=0.001) and normalised in 7 (58%) of the 12 patients with an initially raised level. Serum cholesterol decreased from 6.0 (1.7) to 4.7 (0. 9) mmol/l (p=0.002), LDL-C from 3.5 (1.2) to 2.7 (0.8) mmol/l (p=0. 004), TGs from 4.7 (4.2) to 1.9 (1.0) mmol/l (p=0.001), and C:HDL-C ratios from 6.7 (1.7) to 5.2 (1.0) (p=0.002). HDL-C levels increased insignificantly. High baseline SU, frequency of attacks, total cholesterol, LDL-C and TG levels, and total C:HDL-C ratios correlated with higher decreases in the respective variables upon dietary intervention (p<0.05). CONCLUSION: The results suggest that weight reduction associated with a change in proportional macronutrient intake, as recently recommended in IR, is beneficial, reducing the SU levels and dyslipidaemia in gout. Current dietary recommendations for gout may need re-evaluation.

Adult↗
PubMed1993

Lack of modulation by dietary unsaturated fats on sympathetic neurotransmission in rat hearts.

We examined the effect of dietary polyunsaturated fatty acids (PUFA) on cardiac sympathetic neurotransmission. Rats were fed semisynthetic diets (18.5% fat wt/wt) high in saturated fatty acids (control diet), high in n-6 PUFA (corn oil), or enriched with n-3 PUFA (Maxepa). A perfused innervated heart model was used to examine different aspects of sympathetic neurotransmission 10 wk after the feeding. Dietary PUFA increased the content of n-6 or n-3 PUFA in myocardial phospholipids compared with animals fed control diets. Myocardial norepinephrine content, sympathetic nerve stimulation-induced norepinephrine release, neural reuptake, presynaptic alpha-adrenergic inhibition of norepinephrine release, and postsynaptic inotropic response (+/- dP/dt) to sympathetic nerve stimulation or to a beta-agonist were essentially not influenced by dietary PUFA. Neural norepinephrine release during prolonged ischemia (60 min) was also similar in hearts from rats fed n-6 PUFA and control diets. Thus a modification of sympathetic neurotransmission was not achieved by feeding PUFA-enriched diets for 10 wk.

Animals↗