Dietary protein effects on lipoproteins and on sex and thyroid hormones in blood of rhesus monkeys

We studied plasma lipoprotein and hormone concentrations in rhesus monkeys that had consumed either a low protein (3.8% of kilocalories) or a control protein (13.9%) purified diet since birth (6-10 yr before the beginning of this experiment) in order to test the hypothesis that chronic protein deficiency could influence plasma lipoproteins through an effect on the hepatic metabolism of gonadal or thyroid hormones. Protein-deficient monkeys had greater plasma concentrations of very low density lipoproteins (VLDL) plus high density lipoproteins (HDL) than controls. They also had lower serum albumin and greater alkaline phosphatase levels than the controls. Plasma thyroxine (T4) and free T4 concentrations were lower and the triiodothyronine (T3) levels tended to be greater in the protein-deficient group than in controls. This effect was apparent at two widely different levels of dietary iodide. Plasma T3 concentrations were elevated in other adult rhesus monkeys that were fed the low protein diet for only 6 wk. Monkeys injected with estradiol benzoate (100 micrograms/kg body weight) for 4 d had a marked reduction of VLDL concentrations. VLDL triglycerides were depressed more and plasma estrone levels were greater in deficient monkeys than in controls at 24 h after the last injection. In the control monkeys the T3 level rose and T4/T3 fell in response to estrogen injections, whereas the deficient monkeys did not respond.     

Effect of protein, unsaturated fat, and carbohydrate intakes on plasma apolipoprotein B and VLDL and LDL containing apolipoprotein C-III: results from the OmniHeart Trial

BACKGROUND: Plasma apolipoprotein B (apo B) and VLDL and LDL with apolipoprotein C-III (apo C-III) are independent risk factors for cardiovascular disease (CVD). Dietary intake affects lipoprotein concentration and composition related to those apolipoproteins. OBJECTIVE: We studied differences in apo B lipoproteins with and without apo C-III after 3 healthy diets based on the Dietary Approaches to Stop Hypertension Trial diet. DESIGN: Healthy participants (n = 162) were fed each of 3 healthy diets for 6 wk in a crossover design. Diets differed by emphasis of either carbohydrate (Carb), unsaturated fat (Unsat), or protein (Prot). Blood was collected at baseline and after diets for analysis. RESULTS: Compared with the Carb diet, the Prot diet reduced plasma apo B and triglycerides in VLDL with apo C-III (16%, P = 0.07; 11%, P = 0.05, respectively) and apo B in LDL with apo C-III (16%, P = 0.04). Compared with the Unsat diet, the Prot diet reduced triglycerides in VLDL with apo C-III (16%, P = 0.02). Compared with baseline (subjects' usual diet was higher in saturated fat), the Prot diet reduced apo B in LDL with apo C-III (11%, P = 0.05), and all 3 diets reduced plasma total apo B (6-10%, P < 0.05) and apo B in the major type of LDL, LDL without apo C-III (8-10%, P < 0.01). All 3 diets reduced the ratio of apo C-III to apo E in VLDL. CONCLUSIONS: Substituting protein for carbohydrate in the context of a healthy dietary pattern reduced atherogenic apo C-III-containing LDL and its precursor, apo C-III-containing VLDL, resulting in the most favorable profile of apo B lipoproteins. In addition, compared with a typical high-saturated fat diet, healthy diets that emphasize carbohydrate, protein, or unsaturated fat reduce plasma total and LDL apo B and produce a lower more metabolically favorable ratio of apo C-III to apo E.     

Changes in serum and lipoprotein fatty acids of growing rats fed protein-deficient diets with low or adequate linolenic acid concentrations.

The effects of a protein-deficient diet associated with sunflower oil [adequate in 18:2(n-6), poor in 18:3(n-3)] or soybean oil [adequate in both 18:2(n-6) and 18:3(n-3)] on lipid serum and lipoprotein compositions were studied in growing rats. Four groups of rats were fed different diets: SFC (20% casein + 5% sunflower oil); SFd (2% casein + 5% sunflower oil); SC (20% casein + 5% soybean oil); Sd (2% casein + 5% soybean oil). After 28 d, both protein-deficient groups exhibited low concentrations of protein, phospholipid, triacylglycerol and total cholesterol in serum and VLDL. Compared with rats fed 20% casein diets, those fed low protein diets had lower 18:2(n-6) and 20:4(n-6) in phospholipids of serum, VLDL and HDL2-3, and the 20:4(n-6)/18:2(n-6) ratio was twofold higher in triacylglycerols of serum and VLDL. In the SFd-fed group, 22:5(n-6) was higher than in the SFC-fed group for both triacylglycerols and phospholipids in overall lipoprotein fractions studied. In addition, the 20:3(n-9)/20:4(n-6) ratio was 0.1 in HDL2-3 phospholipids of the SFd-fed group. Sunflower oil-fed rats compared with soybean oil-fed rats had greater monounsaturated fatty acids and lower total (n-3) fatty acids in both triacylglycerols and phospholipids of serum, VLDL and HDL2-3, as well as lower total (n-6) fatty acids in serum and VLDL triacylglycerols. Apolipoproteins (apo) of VLDL were drastically depressed in rats fed protein-deficient diets, whereas apo-AI of HDL2-3 showed a particular resistance. Likewise, sunflower oil-fed rats had enhanced apo-B48 of VLDL and apo-C, apo-AII and apo-AIV of HDL2-3. The present findings show that some effects of protein malnutrition were enhanced by alpha-linolenic acid deficiency, in particular reduced (n-6) and (n-3) fatty acid bioavailability.     

Time course of changes in rat serum apolipoproteins during the consumption of different low protein diets followed by a balanced diet

The effects of protein malnutrition (PM) followed by refeeding a balanced diet on apolipoprotein and lipid contents of the serum lipoproteins were studied in young Wistar male rats. The changes of serum apolipoproteins were compared with the appearance of fatty liver during PM and its disappearance during refeeding. The control group (T) was fed a balanced diet containing 15% casein for 42 d. Two depleted groups (C) and (G1) were fed for 28 d low protein diets containing 2% casein and 5% gluten, respectively, and then were fed the balanced diet for 14 d. During PM a concentration of triacylglycerols (TGs) in liver in the two depleted groups increased; the level in rats fed 2% casein was twice that in rats fed 5% gluten. There was a significant negative correlation between serum TGs and liver TGs. The serum apolipoproteins (apo) did not respond consistently. The high-density lipoproteins apo A-I, A-II and A-IV, which are more than 50% synthetized in the intestine, remained essentially unchanged, thus showing resistance to protein malnutrition. The very low density lipoproteins apo B and total apo C, which mainly originate from liver, were significantly lower in malnourished groups than in controls, while the liver TGs accumulated in malnourished groups. Only the levels of total apo C and apo B48 were correlated with hepatic TG steatosis during malnutrition and refeeding.     

Plasma lipoprotein profile in fasted and refed chickens of two strains selected for high or low adiposity

The plasma lipoprotein profile has been determined in fasted and refed 5-week-old male broilers selected for low or high adiposity. Lipoprotein classes were subfractionated by density gradient ultracentrifugation, appearing as distinct bands with the following densities: very low density lipoprotein (VLDL), d less than 1.013 g/ml; low density lipoprotein (LDL), d 1.023-1.046 g/ml and high density lipoprotein (HDL), d 1.052-1.130 g/ml; the physiochemical characteristics (chemical composition, electrophoretic mobility and particle size) of these particles were then assessed. HDL, seen as a single band, represented 80% of total lipoproteins, with VLDL and LDL accounting for 1% and 16%, respectively, in fasted birds. Lipoprotein profiles were similar in fasted and refed animals of both lines, with the exception that VLDL levels were some 14-fold and 7-fold higher in the lean and fat lines, respectively, in the refed state. The VLDL of fasted birds of both lines were enriched in protein and relatively homogeneous in size; by contrast, VLDL in the refed state contained more triglyceride and less cholesteryl ester and protein and were larger and more heterogeneous, possibly representing a mixture of portomicrons and VLDL of hepatic origin. Birds of the fat line in both nutritional states differed from lean birds in exhibiting elevated plasma lipid and lipoprotein [VLDL, intermediate density lipoprotein (IDL) and HDL] levels, evidence that liver activity is directed toward increased lipoprotein production and secretion in that line.     

Apolipoprotein C-II modifications associated with an infusion of artificial lipid particles

Artificial lipid particles used as parenteral nutrition solution do not contain any apolipoproteins when they are infused into the circulation. Despite the absence of apolipoproteins, the metabolism of artificial lipid particles is similar to that of chylomicrons which contain various kinds of apolipoprotein. Of the known apolipoproteins, apolipoprotein C-II (apo C-II) is important in the hydrolysis of triglyceride-rich lipoproteins via involvement in the activation of lipoprotein lipase. Modifications of apo C-II associated with intravenous infusion of a lipid emulsion were investigated in eight patients. Changes in apo C-IIs in high density lipoproteins (HDL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) together with the plasma level of triglycerides, were quantified before and for 90 min after a bolus injection of a 10% lipid emulsion (1 ml/kg of body weight). Immediately prior to the injection, 54% of the total amount of apo C-II was present in HDL, while 27% was present in VLDL. After 5 to 10 min, the amount of apo C-II in HDL decreased to 29% of the total, while that in VLDL increased to 62%. Subsequently, the amounts of apo C-II in HDL and VLDL began to return to the preinjection levels. These variations in apo C-II were closely correlated with the plasma clearance of triglyceride. The result indicates that the injected lipids are not inert particles during their short intravascular life, but that they acquire apo C-II from HDL.     

Responses of plasma lipoproteins and sex hormones to the consumption of lean fish incorporated in a prudent-type diet in normolipidemic men

OBJECTIVE: The effects of lean fish on plasma lipoproteins, postheparin plasma lipolytic activities and sex hormones were examined in 11 normolipidemic male subjects. METHODS: This study was a randomized crossover trial of two isoenergetic prudent-type diets, lean fish diet and beef, pork, veal, eggs and milk (nonfish) diet. Experimental diets provided approximately 11800 kJ--18% as proteins, 50% as carbohydrates, 32% as lipids [ratio of polyunsaturated to saturated fatty acids (P:S) of 1:1 compared with 0.5:1 in preexperimental diet], and 260 mg cholesterol/day. RESULTS: Compared with the nonfish diet, the lean fish diet induced higher plasma total and LDL apolipoprotein (apo) B and apo B:apo A-1 ratio, indicating that the substitution of lean fish for beef, veal, pork, eggs and milk provides little benefits with regard to plasma apo B concentrations in a low-fat high P:S diet. Moreover, triglycerides:apo B and cholesterol:apo B ratios of VLDL were lower following the lean fish diet than the nonfish diet, suggesting the presence of smaller very low-density lipoprotein (VLDL) particles following the consumption of lean fish. Higher plasma concentrations of sex hormone-binding globulin (SHBG), HDL2 cholesterol and HDL2:HDL3 cholesterol ratio were found with the lean fish diet compared with the nonfish diet. Negative correlations between plasma postheparin lipoprotein lipase (LPL) activity and VLDL triglycerides (n = 11, r = -0.53, p = 0.02), and between plasma postheparin LPL activity and VLDL triglycerides:apo B ratio (n = 11, r = -0.64, p = 0.02) were also observed following the lean fish diet. CONCLUSION: These results suggest that the effects of substituting lean fish for beef, veal, pork, eggs and milk on plasma lipoproteins may be partly associated with variations in plasma sex hormone status and plasma LPL activity in normolipidemic men.     

Magnesium deficiency affects plasma lipoprotein composition in rats

Weanling rats were pair-fed for 8 d with control and Mg-deficient diets containing 960 and 30 mg of Mg/kg, respectively. The marked reduction in plasma Mg levels indicated that the rats fed the Mg-deficient diet were indeed deficient. In the Mg-deficient rats the percent composition of triglycerides in VLDL, LDL and HDL was elevated and that of protein was reduced. Although the proportion of cholesterol was reduced in LDL and HDL, that of phospholipid was decreased only in HDL. Magnesium deficiency induced a decrease in the percent composition of apolipoprotein (apo) E and a relative increase in the apo C for VLDL. In HDL from Mg-deficient rats, the proportion of apo AI was higher than normal, apo AIV was lower than normal and apo E was virtually absent. The percent composition of oleic and linoleic acids was increased but that of stearic and arachidonic acids was depressed in both VLDL and HDL derived from Mg-deficient rats compared with pair-fed controls. Whether these alterations in lipoprotein profile contribute to hyperlipoproteinemia or are the results of the metabolic changes that produce hyperlipoproteinemia remain to be determined.     

Effect of chronic glucagon administration on the metabolism of triacylglycerol-rich lipoproteins in rats fed a high sucrose diet

Male adult Wistar rats were fed a semipurified diet rich in sucrose (53 g/100 g diet). The effects of chronic glucagon administration (20 micrograms.day-1.rat-1, for 21 d) were studied on plasma lipid levels, triacylglycerol secretion rates and fractional catabolic rates determined by the intravenous fat tolerance test. Triacylglycerol secretion rates of plasma, chylomicron and very low density lipoprotein (VLDL) were measured by using the Triton WR 1339 method. In both fasting and postprandial states, the different rates were not significantly modified by glucagon treatment. However, in the treated animals, significantly decreased triacylglycerol concentrations were observed in plasma and VLDL during fasting (-41 and -46%, respectively) and also in chylomicrons in the postprandial state (-37%) relative to control animals. These data could be accounted for by an increased removal rate of triacylglycerol-rich lipoprotein. The estimated values of fractional rate constants (Triton WR 1339 experiment) were increased for VLDL (+62%) in the fasting state and for chylomicrons (+104%) in the postprandial state. Similarly, the fractional catabolic rate determined with the intravenous fat tolerance test (Intralipid, Kabivitrum, Sweden) was increased 49% by glucagon treatment, suggesting an effect of glucagon on the catabolism of triacylglycerol-rich lipoproteins. Glucagon treatment did not modify the composition of VLDL obtained 60 min after Triton WR 1339 injection, except that in the fasting state apo B100 proportions and concentrations increased, suggesting a specific effect on the hepatic secretion of apo B100 VLDL.     

Soluble oat fiber tends to normalize lipoprotein composition in cholesterol-fed rats

The effect of oat fiber on VLDL, LDL and HDL composition was investigated by feeding male Sprague-Dawley rats diets containing 1.0% cholesterol and 0.2% cholic acid, and 6% dietary fiber from oat bran, high-fiber oat flour or a processed oat product for 20 d. Compared to cholesterol-fed cellulose controls, all oat fibers altered the response to cholesterol feeding as indicated by 25-45% lower total lipoprotein cholesterol, 40-60% lower VLDL + LDL cholesterol, and 25-40% higher HDL cholesterol contents, P less than 0.01. The effect of the oat fibers on VLDL composition was especially pronounced as demonstrated by 30-65% lower VLDL protein, VLDL apo E and plasma apo B concentrations. The processed oat product which contained 40% more soluble fiber than oat bran or oat flour normalized the lipoprotein profile associated with ingestion of the atherogenic diet significantly more than oat bran or oat flour. Concentration of total lipoprotein cholesterol and distribution of apo E among the VLDL and LDL fractions in the processed oat product group were similar to controls not fed cholesterol. These data indicate that ingestion of oat fiber tends to normalize the lipoprotein profile induced by feeding an atherogenic diet in the rat, and that the hypocholesterolemic effect of oat fiber is associated with its soluble fiber content.     

Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity

BACKGROUND: Lipid abnormalities may contribute to the increased risk of atherosclerosis and coronary disease in visceral obesity. Fish oils lower plasma triacylglycerols, but the underlying mechanisms are not fully understood. OBJECTIVE: We studied the effect of fish oils on the metabolism of apolipoprotein B-100 (apo B) and chylomicron remnants in obese men. DESIGN: Twenty-four dyslipidemic, viscerally obese men were randomly assigned to receive either fish oil capsules (4 g/d, consisting of 45% eicosapentaenoic acid and 39% docosahexaenoic acid as ethyl esters) or matching placebo (corn oil, 4 g/d) for 6 wk. VLDL, intermediate-density lipoprotein (IDL), and LDL apo B kinetics were assessed by following apo B isotopic enrichment with the use of gas chromatography-mass spectrometry after an intravenous bolus injection of trideuterated leucine. Chylomicron remnant catabolism was measured with the use of an intravenous injection of a chylomicron remnant-like emulsion containing cholesteryl [(13)C]oleate, and isotopic enrichment of (13)CO(2) in breath was measured with isotope ratio mass spectrometry. Kinetic values were derived with multicompartmental models. RESULTS: Fish oil supplementation significantly (P < 0.05) lowered plasma concentrations of triacylglycerols (-18%) and VLDL apo B (-20%) and the hepatic secretion of VLDL apo B (-29%) compared with placebo. The percentage of conversions of VLDL apo B to IDL apo B, VLDL apo B to LDL apo B, and IDL apo B to LDL apo B also increased significantly (P < 0.05): 71%, 93%, and 11%, respectively. Fish oils did not significantly alter the fractional catabolic rates of apo B in VLDL, IDL, or LDL or alter the catabolism of the chylomicron remnant-like emulsion. CONCLUSION: Fish oils effectively lower the plasma concentration of triacylglycerols, chiefly by decreasing VLDL apo B production but not by altering the catabolism of apo B-containing lipoprotein or chylomicron remnants.     

Increased plasma concentrations of lipoprotein(a) during a low-fat, high-carbohydrate diet are associated with increased plasma concentrations of apolipoprotein C-III bound to apolipoprotein B-containing lipoproteins

BACKGROUND: Low-fat, high-carbohydrate (LFHC) diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)] and of triacylglycerol- rich lipoproteins (TRLs). OBJECTIVE: We tested whether increases in plasma Lp(a) induced by an LFHC diet are related to changes in TRLs. DESIGN: Healthy men (study 1; n = 140) consumed for 4 wk each a high-fat, low-carbohydrate diet (HFLC; 40% fat, 45% carbohydrate) and an LFHC diet (20% fat, 65% carbohydrate). Plasma lipids; lipoproteins; apolipoprotein (apo) B, A-I, and C-III; and Lp(a) were measured at the end of each diet. In a second group of men following a similar dietary protocol (study 2; n = 33), we isolated apo(a)-containing particles by immunoaffinity chromatography and determined the concentrations of apo C-III in ultracentrifugally isolated subfractions of apo B-containing lipoproteins. RESULTS: In study 1, plasma concentrations of Lp(a) (P < 0.001), triacylglycerol (P < 0.001), apo B (P < 0.005), apo C-III (P < 0.005), and apo C-III in apo B-containing lipoproteins (non-HDL apo C-III) (P < 0.001) were significantly higher with the LFHC diet than with the HFLC diet. Stepwise multiple linear regression analysis showed that the association of changes in Lp(a) with changes in non-HDL apo C-III was independent of changes in body mass index, apo B, LDL cholesterol, and HDL cholesterol. Plasma lipid and lipoprotein changes were similar in study 2, and we found that both total apo C-III and the apo C-III content of apo(a)-containing particles were increased in a TRL fraction consisting predominantly of large VLDL particles [TRL-apo(a)]. CONCLUSIONS: The increase in plasma Lp(a) with an LFHC diet is significantly associated with an increase in non-HDL apo C-III. Enrichment of TRL-apo(a) with apo C-III may contribute to this dietary effect on Lp(a) concentrations.     

Adipose tissue lipogenesis and fat deposition in leaner broiler chickens.

Rates of hepatic lipogenesis and secretion of plasma triglyceride-rich lipoproteins in 6- to 7-wk-old broiler chickens were similar to the overall rate of fat deposition in these birds, although approximately 20% of [14C]-labeled VLDL was oxidized to CO2 within 8 h. Only 6-7% of VLDL and portomicron triglyceride was taken up by the abdominal fat pad, but this proportion of total triglyceride flux could account for about 80-85% of the total fatty acids accumulating in that depot. The rate of lipogenesis in adipose tissue was much lower than that in the liver, but it could account for much of the remaining fatty acids. Lipogenesis from [14C]acetate in cultured chicken adipocytes was markedly inhibited by adding VLDL as an exogenous source of fatty acids. However, adipose tissue lipogenesis was not increased in vivo by reduction of plasma lipoprotein flux by genetic selection, by the feeding of a high protein diet or by immunological intervention. The results confirm that adipose tissue lipogenesis makes only a small contribution to adipose tissue growth in normal broilers. Its importance does not increase in response to the reductions in hepatic lipogenesis that accompany genetic or nutritional manipulation of body composition.     

The coffee diterpene cafestol increases plasma triacylglycerol by increasing the production rate of large VLDL apolipoprotein B in healthy normolipidemic subjects

BACKGROUND: Cafestol is a diterpene in unfiltered coffee that raises plasma triacylglycerol in humans. OBJECTIVE: We studied whether cafestol increases plasma triacylglycerol by increasing the production rate or by decreasing the fractional catabolic rate of VLDL(1) [Svedberg flotation unit (S(f)) 60-400] apolipoprotein (apo) B. In addition, we studied the effect of cafestol on the composition of VLDL(1) and VLDL(2) (S(f) 20-60). DESIGN: Eight healthy normolipidemic men were administered a daily dose of 75 mg cafestol for 2 wk. A bolus injection of 7 mg L-[5,5,5-(2)H(3)]leucine/kg body wt was given after a baseline period with no cafestol and again after treatment with cafestol. We derived kinetic constants to describe the metabolism of VLDL(1) apo B by using a multicompartmental model. RESULTS: Cafestol significantly increased plasma triacylglycerol by 31% or 0.32 mmol/L (95% CI: 0.03, 0.61); the increase was due mainly to a nonsignificant rise in VLDL(1) triacylglycerol of 57% or 0.23 mmol/L (95% CI: -0.02, 0.48). Cafestol significantly increased the mean rate of VLDL(1) apo B production by 80% or 755 mg/d (95% CI: 0.2, 5353), whereas it did not significantly change the mean fractional catabolic rate of VLDL(1) apo B (mean increase of 3 pools/d; 95% CI: -4, 10]). Cafestol did not change the composition of VLDL(1). A significant increase in the ratio of VLDL(2) cholesteryl ester to triacylglycerol indicates that VLDL(2) became enriched with cholesteryl esters at the cost of triacylglycerol. CONCLUSION: Cafestol increases plasma triacylglycerol by increasing the production rate of VLDL(1) apo B, probably via increased assembly of VLDL(1) in the liver.     

Effect of beta-carotene supplementation on the concentrations and distribution of carotenoids,vitamin E,vitamin A,and cholesterol in plasma lipoprotein and non-lipoprotein fractions in healthy older women.

We studied the effect of beta-carotene supplementation on the concentrations and distribution in plasma lipoprotein and non-lipoprotein fractions of carotenoids, alpha-tocopherol, retinol, and cholesterol.

Ten women ingested either 90 mg of beta-carotene or placebo daily for 3 weeks while residing in their homes and eating their usual meals. Carotenoids (beta-carotene, lycopene, lutein/zeaxanthin), retinol, alpha-tocopherol, and cholesterol were measured in plasma lipoprotein and non-lipoprotein fractions before and after treatment.

In the beta-carotene-supplemented group, total plasma beta-carotene increased 14-fold from 0.48 +/? 0.13 to 6.83 +/? 2.12 mumol/L (p = 0.04). Although the greatest increase in beta-carotene was in low-density-lipoproteins (LDL), the magnitude of increase was similar in LDL, high-density-lipoproteins (HDL), and very-low-density-lipoproteins (VLDL). Thus, the relative distribution of beta-carotene in lipoproteins was unchanged: approximately 71% was in LDL, approximately 15% in HDL and approximately 12% in VLDL, before and after beta-carotene supplementation. There were no changes in amounts and distribution in lipoproteins of the other carotenoids, alpha-tocopherol, and cholesterol. There was no change in the amount of retinol in lipoprotein-deficient plasma. There were no changes in total plasma triglycerides. Significant positive correlations were found between LDL- or VLDL-cholesterol and alpha-tocopherol in LDL or VLDL, respectively; between LDL- or VLDL-cholesterol and lutein/zeaxanthin in LDL or VLDL, respectively; and between HDL-cholesterol and beta-carotene in HDL.

beta-Carotene supplementation (90 mg/day for 3 weeks) in healthy older women results in an enrichment of all plasma lipoprotein fractions with beta-carotene, but does not alter the relative distribution of beta-carotene in lipoproteins. beta-Carotene supplementation has no effect on the amounts and relative distribution of lycopene, lutein/zeaxanthin, and alpha-tocopherol in lipoproteins, or of retinol in the non-lipoprotein fraction of plasma. Short-term beta-carotene supplementation has no effect on the concentrations of plasma total triglycerides, total cholesterol, HDL-, LDL-, and VLDL-cholesterol.     

Responses of Plasma Lipoproteins and Sex Hormones to the Consumption of Lean Fish Incorporated in a Prudent-Type Diet in Normolipidemic Men

Objective: The effects of lean fish on plasma lipoproteins, postheparin plasma lipolytic activities and sex hormones were examined in 11 normolipidemic male subjects.

Methods: This study was a randomized crossover trial of two isoenergetic prudent-type diets, lean fish diet and beef, pork, veal, eggs and milk (nonfish) diet. Experimental diets provided approximately 11800 kJ—18% as proteins, 50% as carbohydrates, 32% as lipids [ratio of polyunsaturated to saturated fatty acids (P:S) of 1:1 compared with 0.5:1 in preexperimental diet], and 260 mg cholesterol/day.

Results: Compared with the nonfish diet, the lean fish diet induced higher plasma total and LDL apolipoprotein (apo) B and apo B:apo A-1 ratio, indicating that the substitution of lean fish for beef, veal, pork, eggs and milk provides little benefits with regard to plasma apo B concentrations in a low-fat high P:S diet. Moreover, triglycerides:apo B and cholesterol:apo B ratios of VLDL were lower following the lean fish diet than the nonfish diet, suggesting the presence of smaller very low-density lipoprotein (VLDL) particles following the consumption of lean fish. Higher plasma concentrations of sex hormone-binding globulin (SHBG), HDL₂ cholesterol and HDL₂:HDL₃ cholesterol ratio were found with the lean fish diet compared with the nonfish diet. Negative correlations between plasma postheparin lipoprotein lipase (LPL) activity and VLDL triglycerides (n = 11, r = ?0.53, p = 0.02), and between plasma postheparin LPL activity and VLDL triglycerides:apo B ratio (n = 11, r = ?0.64, p = 0.02) were also observed following the lean fish diet.

Conclusion: These results suggest that the effects of substituting lean fish for beef, veal, pork, eggs and milk on plasma lipoproteins may be partly associated with variations in plasma sex hormone status and plasma LPL activity in normolipidemic men.     

Hepatic steatosis and serum very low density lipoproteins during two types of protein malnutrition followed by balanced refeeding

The relation of serum very low density lipoproteins (VLDL) to hepatic steatosis was studied during protein malnutrition followed by refeeding of a balanced diet in growing rats. A control group was fed a balanced diet containing 15% casein for 42 days. Two depleted groups were fed low protein diets containing 2% casein (group C) or 5% gluten (group GI) (protein malnutrition phase) for 28 days and then were fed the balanced diet for 14 days (refeeding phase). The concentrations of phospholipids and proteins in both liver and serum VLDL were decreased during protein malnutrition, whereas triacylglycerols, unesterified cholesterol, and cholesteryl esters were higher in the liver and lower in the serum VLDL in the C and GI groups compared with the control group. There was a significant inverse relation between serum VLDL apolipoproteins and liver triacylglycerols on the one hand and between serum VLDL triacylglycerols and liver triacylglycerols on the other hand, in both depleted groups, although this relation was less important in the GI group. The major fatty acid levels of liver triacylglycerols were negatively correlated with those of serum VLDL during protein malnutrition. Our results show that in spite of a similar fatty acid intake, protein malnutrition involved an important decrease in essential fatty acids in VLDL triacylglycerols and phospholipids. Moreover, triacylglycerol accumulation was accompanied by increases in unesterfied cholesterol and cholesteryl esters in the liver of rats fed low protein diets, especially with 5% gluten. Hence, the hepatic steatosis was not entirely attributable to impaired transport of triacylglycerols by VLDL.     

Interrelationship of plasma triglycerides and HDL size and composition in rats fed different dietary saturated fats

We investigated the relative effects of different dietary saturated fats on the size distribution, apolipoprotein (apo) and chemical composition of HDL in fasted rats. Male Sprague-Dawley rats (174 +/- 2 g) were fed diets containing 0.035% cholesterol and 16% fat (wt/wt) from corn oil (CO diet) or from 2% CO plus 14% butterfat (BF diet), beef tallow (BT diet), palm oil (PO diet) or coconut oil (CN diet) for 6 wk. Apparent lipid digestibility was significantly lower with the PO and BT diets vs. the CO, BF and CN diets. Plasma total cholesterol levels were significantly higher in rats fed the PO and BT diets than in rats fed the BF and CN diets but were not different among the PO-, BT- and CO-fed groups. Nondenaturing gradient gel electrophoresis immunoblot analysis indicated that HDL apo A-I and E resided on particles with significantly smaller modal diameters in rats fed all saturated fats compared with those fed the CO diet. Chemical analyses indicated that HDL generally contained proportionately less protein and more triglyceride, free cholesterol and apo E with saturated fat feeding than with CO diet feeding. Significantly higher plasma and VLDL triglyceride levels were noted with ingestion of the BT, PO or CN diet than with the CO diet. Butterfat feeding resulted in lower plasma triglycerides and HDL-esterified cholesterol than did feeding the other saturated fats. Very low density lipoprotein triglyceride concentrations were inversely correlated with HDL modal diameter of apo E containing lipoproteins (P less than 0.005). These data provide further evidence of the interrelationship of triglyceride and HDL metabolism and suggest that mechanisms independent of cholesterol ester transfer protein may mediate this response in rats.     

Thyroid function, energy balance, body composition and organ growth in protein-deficient chicks

Protein-deficient diets (17, 10, 6.5 or 3% protein) and a 24% control diet were fed to growing chicks. A control group was pair-fed daily with each deficient group. Energy intake was lower in the 6.5 and 3% protein groups than in the other groups. However, weight gain, bone growth and feed conversion efficiency were lower with 10% protein or less. Relative thyroid weights were unaffected by dietary protein. Plasma T3 (3,5,3'-triiodothyronine) levels were significantly higher in all deficient groups, whereas plasma T4 (thyroxine) was lower. Plasma rT3 (reverse T3) was unaffected by the protein deficiencies, suggesting that enhanced conversion of T4 to T3 rather than to rT3 had occurred. Hepatic alpha-glycerol-3-phosphate dehydrogenase (alpha-GP) shuttle activity increased markedly in protein-deficient chicks. Efficiency of energy utilization was unaltered in chicks fed 17 or 10% protein but was higher in chicks fed 6.5 and 3% protein than in controls. All deficient chicks had more fat and less protein and water in the tissues. The lower feed conversion efficiency therefore represents almost entirely a shift in body composition toward fat and does not reflect a loss of energy as heat. We conclude that elevations in plasma T3 and in thyroid-controlled alpha-GP shuttle activity, although sensitive indicators of protein deficiencies, are not good predictors of altered thermogenic activity in protein-deficient chicks.     

Modifications of hemato-biological parameters in pregnant women in a migrating population in northern Cameroon: prevalence of anemia, iron and folates deficiencies

The wholesale displacement of a population can have nutritional consequences for the migrants. With this in mind, the prevalences of anemia and of iron and folic acid deficiencies were studied in a group of 90 pregnant women living in northeast Benoue, an area situated in northern Cameroon where a development project was initiated in 1973. This project aimed at moving a population from the extreme northern highlands to the fertile valley of the Benoue. The following hemato-biological parameters were measured: hemoglobin, hematocrit, mean cell hemoglobin concentration, plasma iron, transferrin saturation, serum concentrations of folates, prealbumin, transferrin, protides and their fractions. The investigation showed that anemia, as well as iron and folic acid deficiencies, were rare when using World Health Organization criteria. The anemia prevalence, judged on a hemoglobin level of less than 11 g per 100 ml, is 8%, iron deficiency prevalence is 10% (plasma iron level below 50 micrograms per 100 ml), and folic acid deficiency prevalence is 3% (serum folic acid level below 3 ng per ml). However, 40% of the pregnant women had a level of transferrin saturation below 15%. In non deficient subjects, we observed a decrease between the first and second trimesters of pregnancy in hemato-biological parameters linked to anemia or to nutritional status (hemoglobin, hematocrit, plasma iron, transferrin saturation, prealbumin). The nutritional conditions in the area appeared sufficient to prevent deficiencies which are frequently observed in pregnant women in Africa.