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S Moorjani

Publications and source records attributed to S Moorjani.

At least 37 records · Page 2Linked to original sources

Plasma high-density lipoprotein cholesterol but not apolipoprotein A-I is a good correlate of the visceral obesity-insulin resistance dyslipidemic syndrome.

Apolipoprotein (apo) A-I is a major component of high-density lipoproteins (HDLs), and it has been suggested that measurement of apo A-I may provide additional information in the assessment of coronary heart disease (CHD) risk. In the present study in a sample of 111 men (age [mean +/- SD], 35.3 +/- 6.6 years), we determined whether a low apo A-I concentration is associated with the cluster of metabolic abnormalities that characterize the visceral obesity-insulin resistance dyslipidemic syndrome. For this purpose, the first and fourth quartiles of apo A-I and HDL cholesterol (HDL-C) concentrations were compared in relation to body fat distribution, glucose tolerance, and plasma insulin and lipoprotein levels. Men in the first quartile (< the 25th percentile) of HDL-C, as compared with men in the fourth quartile (> the 75th percentile), were characterized by an elevated visceral adipose tissue (AT) accumulation (P < .05), as well as by increased plasma levels of triglycerides ([TGs] P < .0001), apo B (P < .0005), and insulin (P < .01). These differences were not found when the first and fourth quartiles of plasma apo A-I concentrations were compared. These results suggest that plasma levels of HDL-C are more closely associated with the various features of the visceral obesity-insulin resistance syndrome than plasma apo A-I.

Adipose Tissue↗

Overfeeding in identical twins: 5-year postoverfeeding results.

From a total of 12 pairs of young male identical twins who were overfed by an estimated 84,000 kcal over a period of 100 days, several pairs (eight to 11, depending on variables) were remeasured for body weight, body composition with the underwater weighing technique, regional fat distribution from skinfolds, girths, computed tomography (CT) fat areas in the abdominal region, and fasting plasma glucose, insulin, total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides 4 months and 5 years after completion of the overfeeding protocol. At 4 months, the twins had lost approximately 7 of 8 kg that they had gained with overfeeding. However, 5 years later, body weight had increased by 5 kg over the preoverfeeding level. Fluctuations in fat mass were greater than those in fat-free mass. The younger twins gained approximately twice as much as the older twins in the late recovery period, a difference attributed to the late phase of growth in body mass in the former. Upper-body fat was reduced at 4 months of follow-up study, but was increased in the late recovery phase. All blood values were normalized in the postoverfeeding periods. A within-pair resemblance was generally observed for the changes noted in the recovery periods, but it was more striking when variations between preoverfeeding and 4-month or 5-year values were considered. We conclude from these observations that there were no persistent effects of exposure to the overfeeding protocol over the expected age-associated increases in body mass, body fat, upper-body fat, abdominal visceral fat (AVF), and metabolic variables predictive of risk for common diseases in individuals of normal body weight and with no family history of obesity. The intrapair resemblance suggests that the genotype contributes to the alterations observed in the recovery from overfeeding and in the age-associated changes.

Adipose Tissue↗

Plasma lipoprotein profile and lipolytic activities in response to the substitution of lean white fish for other animal protein sources in premenopausal women.

A crossover study was conducted to examine the effects on plasma lipoprotein concentrations of substituting lean white fish (LWF) for beef, port, veal, eggs, and milk products (BPVEM) within prudent isoenergetic diets. Fourteen premenopausal women received 8784 kJ--20% as protein, 50% as carbohydrates, and 30% as lipids [ratio of polyunsaturated to monounsaturated to saturated fatty acids (P:M:S) of 1:1:1 compared with 0.4:1:1 in preexperimental diet]--and 260 mg cholesterol/d. After 4 wk, the BPVEM diet significantly reduced concentrations of plasma cholesterol, low-density-lipoprotein (LDL) cholesterol, high-density-lipoprotein (HDL) cholesterol, apolipoprotein B, HDL-apolipoprotein A-I, and LDL-apolipoprotein B (P<0.05) as well as plasma postheparin hepatic triacylglycerol lipase activity compared with the preexperimental diet. These effects are probably attributable to elevation of the P:M:S. These responses were not observed with the LWF diet, suggesting that fish protein in LWF maintains unchanged plasma cholesterol concentrations despite a high P:M:S. The LWF diet, compared with the preexperimental diet, reduced very-low-density-lipoprotein triacylglycerol (P<0.05) and also the ratio of LDL cholesterol to apolipoprotein B (P<0.05), revealing the presence of denser LDL particles. Compared with the BPVEM diet, the LWF diet induced lower concentrations of very-low-density-lipoprotein triacylglycerols (P<0.05) and higher concentrations of LDL triacylglycerol and LDL apolipoprotein B (P<0.05), which were not associated with any increase in lipoprotein lipase activity. These results suggest that LWF as a substitute for BPVEM in isoenergetic diets with an elevated P:S produces minimal improvement in the lipoprotein profile in premenopausal women.

Adult↗

The apoB-100 gene EcoRI polymorphism influences the relationship between features of the insulin resistance syndrome and the hyper-apoB and dense LDL phenotype in men.

The aim of this study was to investigate whether the EcoRI polymorphism of the apolipoprotein B (apoB) gene influences the relationships between features of the insulin resistance syndrome and the dense LDL phenotype and apoB concentrations. A sample of 65 men was divided into two groups on the basis of the EcoRI genotype. Forty-four subjects were (+/+) homozygotes for the presence of the EcoRI restriction site that is associated with a glutamic acid at codon 4154. Twenty-one men were (+/-) heterozygotes for the absence of the restriction site resulting from a glutamic acid to a lysine substitution at codon 4154. In the (+/-) group, fasting plasma FFA levels were positively correlated with plasma apoB, LDL-apoB, and the LDL particle score that was calculated from the migration distances of LDL subspecies and their relative band intensities, reflecting the proportion of small dense LDL particles. However, these associations were not found among (+/+) subjects. The two genotypic groups were further divided into two subgroups on the basis of fasting FFA concentrations, and the LDL particle score and the LDL-apoB levels were compared. High FFA levels were associated with a higher proportion of small dense LDL particles, as reflected by a higher mean LDL particle score, irrespective of the genotype. However, the apoB-EcoRI polymorphism appeared to influence the association between high FFA levels and LDL-apoB concentrations because (+/-) heterozygotes with high FFA levels had higher LDL-apoB concentrations than (+/-) heterozygotes with low FFA levels. In addition, the integrated area under the curve of plasma insulin concentrations, measured in response to a 75-g oral glucose challenge, and the amount of visceral adipose tissue, measured by computed tomography, were positively associated with the LDL particle score only in (+/-) heterozygotes. When subjects were divided on the basis of insulin area (low vs. high) or visceral adipose tissue (low vs. high), (+/-) heterozygotes with high insulin area or with high levels of visceral adipose tissue had a higher mean LDL particle score than (+/-) heterozygotes with low insulin area or low visceral adipose tissue. However, among (+/+) homozygotes, low or high levels of insulin or visceral adipose tissue could not discriminate between men with large or small LDL particles. Therefore, (+/-) heterozygotes may be more susceptible to develop the dense LDL phenotype in presence of hyperinsulinemia and visceral obesity. Results of the present study suggest that the apoB-EcoRI polymorphism may exacerbate the alterations in the LDL particle (size and concentration) found among visceral obese-hyperinsulinemic men.

Adipose Tissue↗

The dense LDL phenotype. Association with plasma lipoprotein levels, visceral obesity, and hyperinsulinemia in men.

OBJECTIVE: To investigate the potential relationship between the cluster of metabolic abnormalities found in visceral obesity and the small dense LDL phenotype. RESEARCH DESIGN AND METHODS: We have estimated LDL peak particle size by nondenaturing 2-16% gradient gel electrophoresis in a sample of 79 men. Glucose tolerance and fasting plasma insulin and lipoprotein levels were also measured. RESULTS: The LDL particle score, calculated from migration, distances and relative band intensities and reflecting the proportion of small dense LDL particles, was positively correlated with plasma triglyceride (TG) (r = 0.60, P < 0.0001) and negatively correlated with HDL cholesterol (r = -0.56, P < 0.0001) levels. Although the LDL particle score was not associated with variations in plasma LDL cholesterol or LDL apolipoprotein (apo) B concentrations, it was significantly correlated with the LDL apo B-to-LDL cholesterol ratio (r = 0.60, P < 0.0001). Fasting plasma insulin and visceral adipose tissue (AT) areas measured by computed tomography were weakly but significantly correlated with the LDL particle score (r = 0.23 and 0.29, respectively, P < 0.05). LDL peak particle size showed similar but inverse correlations with anthropometric and metabolic variables. Subjects classified as having small dense LDL particles (by comparing subjects in the highest tertile versus those in the lowest tertile of the LDL particle score distribution) were characterized by increased plasma TG, reduced HDL cholesterol, higher fasting insulin levels, and elevated visceral AT accumulation. However, multiple regression analyses revealed that visceral AT accumulation was not an independent predictor of the dense LDL phenotype after inclusion of TG and HDL cholesterol levels and lipoprotein ratios in the model. CONCLUSIONS: It thus appears that the high TG-low HDL cholesterol dyslipidemia frequently found in visceral obesity and in a hyperinsulinemic state is a strong correlate of the small dense LDL phenotype. Although associated with the dense LDL phenotype, visceral obesity and hyperinsulinemia were not independent predictors of an increased proportion of small dense LDL particles after controlling for TG and HDL cholesterol levels.

Adipose Tissue↗

Alterations in plasma lipoproteins and apolipoproteins before the age of 40 in heterozygotes for lipoprotein lipase deficiency.

We have assessed the expression of heterozygosity for lipoprotein lipase (LPL) deficiency by studying a single large French Canadian family comprising 92 persons including 21 carriers of the catalytically defective P207L mutation. Phenotypic changes distinguishing heterozygotes from controls were seen early, before the age of 40 and often before 20 years of age. In the total cohort these changes included an elevation in the mean very low density (VLDL) and intermediate density lipoprotein (IDL) triglyceride (+69%; P = 0.01 and +40%; P = 0.001) and cholesterol (+51%; P = 0.03 and +67%; P = 0.007) and apoB levels but decreased HDL2 and HDL3 cholesterol, (-32%; P = 0.01 and -15%; P = 0.002 respectively). While the lipid compositions of VLDL and IDL were similar between heterozygotes and controls, the low density (LDL) and high density lipoproteins (HDL) of carriers were triglyceride enriched. Heterozygotes also had a markedly lower apoC-III ratio (apoC-III in supernatant/apoC-III in heparin precipitate) (1.46 vs. 3.86 P = 1 x 10(-4)) indicating a substantial enrichment of VLDL and IDL with apoC-III and depletion of HDL apoC-III supporting this ratio as an effective index for efficiency of lipolysis. LpA-I was markedly reduced (0.34 vs. 0.43 P = 1 x 10(-5)) showing that levels of this particle are partly dependent on LPL catalytic activity. Heterozygotes manifest from an early age with a markedly reduced HDL, LpA-I, apoC-III ratio and an increased TC/HDLc ratio which would predict a relatively increased risk of premature coronary artery disease, compared to their normal siblings.

Adult↗

Associations between 12 year changes in body fatness and lipoprotein-lipid levels in men and women of the Québec Family Study.

OBJECTIVE: To investigate the associations between 12 year changes in body composition, subcutaneous fat distribution vs changes in plasma lipoprotein-lipid levels. DESIGN: 12 year prospective study. SUBJECTS: A sample of 95 women and 93 men of the Québec Family Study initially tested in 1980. MEASUREMENTS: Various body fatness variables as well as fasting plasma lipoprotein-lipid concentrations performed both in 1980 and 1992. RESULTS: In both 1980 and 1992, a high body fat mass and an elevated accumulation of subcutaneous trunk fat were associated with a significant deterioration in the plasma lipoprotein-lipid profile. Furthermore, correlation analysis performed on differences noted during the 12 years follow-up revealed significant associations between changes in body fat mass and in plasma cholesterol [r = 0.52, P < 0.0005] in women. In both men and women, an increased body fat mass was associated with an increased CHOL/HDL-cholesterol ratio [r = 0.37, P < 0.01 (men) and r = 0.54, P < 0.0005 (women)]. Correlations between changes in fat mass and plasma lipids were generally of higher magnitude in women than in men. Changes in subcutaneous trunk fat were associated with changes in plasma HDL-chol levels (r = -0.22, P < 0.05) in men whereas in women, changes in trunk adiposity were related to changes in both plasma CHOL (r = 0.25, P < 0.05) and TG (r = 0.32, P < 0.005) levels. CONCLUSION: These results support the notion that the increased adiposity observed among aging adult men and women is a significant component of the deterioration in the plasma lipoprotein-lipid profile noted over a 12 year follow-up period.

Adipose Tissue↗

Prevalence of dyslipidemic phenotypes in ischemic heart disease (prospective results from the Québec Cardiovascular Study)

In 1985, plasma cholesterol, triglyceride, high-density lipoprotein cholesterol, and plasma apoprotein (apo) B levels were measured in 2,103 men (aged 45 to 76 years) without ischemic heart disease from the Québec city suburbs. Occurrence of a first ischemic event (i.e., angina pectoris, acute myocardial infarction, or coronary-related death) was recorded in 114 men between 1985 and 1990. Men with and without ischemic heart disease were classified as normal or in various dyslipidemic groups according to an established algorithm. Of the 1,989 men who remained free of ischemic events, 50% had a normal lipid profile compared with 32% in men with ischemic heart disease. Although the prevalence of type IIb and IV dyslipidemias was similar in men with and without ischemic heart disease, type IIa (16% vs 10%), hyperapo B-hypertriglyceridemia (12% vs 6%), hyperapo B-normotriglyceridemia (11% vs 7%), and hypoalphalipoproteinemia (18% vs 13%) were more prevalent in men with than without ischemic heart disease. Adjusted odds ratios (ORs) were not increased in type IIb and IV phenotypes, whereas men with type IIa (OR 2.8), with the 2 hyperapo B phenotypes (hyperapo B-normotriglyceridemia, OR 2.7; hyperapo B-hypertriglyceridemia, OR 3.1) or with isolated hypoalphalipoproteinemia (OR 2.2), were at higher risk. The results of this prospective study confirm the importance of both elevated plasma cholesterol and decreased high-density lipoprotein cholesterol levels as risk factors for ischemic heart disease. They also emphasize the high prevalence of an elevated apo B dyslipidemic state in ischemic heart disease.

Adult↗

Lipoprotein(a) distribution in a French Canadian population and its relation to intermittent claudication (the Québec Cardiovascular Study)

This study was undertaken to evaluate the distribution and the relation of lipoprotein(a) (Lp[a]) concentration with intermittent claudication in a cohort of men aged 35 to 64 years, randomly selected in 1974 and followed until 1990. In 1985, blood samples for a complete fasting lipid profile and Lp(a) were obtained in 2,424 men representing 62% of the living cohort. The diagnosis of intermittent claudication was made by trained nurses using a standardized questionnaire and confirmed by a cardiologist. Lp(a) distribution did not change with age and was similar to that of other Caucasian populations. Because Lp(a) concentration did not vary with age, its relation to the incidence of intermittent claudication was assessed for the years 1974 to 1990. The incidence of intermittent claudication was 42 of 10,000 person-years. The 113 men with intermittent claudication, in contrast to men without this symptomatology, were older at entry (49 +/- 7 vs 45 +/- 7 years), and had higher systolic pressure (144 +/- 20 vs 136 +/- 16 mmHg) and Lp(a) levels (46 +/- 45 vs 33 +/- 35 mg/dl) (all p < 0.05). There was also a significantly greater prevalence of smoking and diabetes among men with intermittent claudication. The risk of intermittent claudication was doubled in men in the second and third tertiles of Lp(a) concentration (p < 0.001). Thus, high Lp(a) levels constitute a significant risk for intermittent claudication in this population.

Adult↗

Rapid restriction fragment analysis for screening four point mutations of the low-density lipoprotein receptor gene in French Canadians.

Familial hypercholesterolemia (FH) has an estimated frequency of 1:154 among French Canadians in Northeastern Quebec, compared with 1:500 in most other populations. FH is caused by numerous mutations of the low-density lipoprotein (LDL) receptor gene, but only six well-characterized mutations are known to cause FH in French Canadians. High prevalence of the phenotype, along with a limited number of mutations in this population, provides a unique opportunity to study genotype-phenotype variation. Since the current methods for detection of point mutations in this population use complicated approaches, we report polymerase chain reaction (PCR)-based restriction fragment analysis to detect all four point mutations. This approach provides a rapid diagnosis and is suitable to screen large number of samples for studies in genetic epidemiology; it should be useful in identifying FH in other populations bearing the same mutations.

Base Sequence↗

Do elevated levels of abdominal visceral adipose tissue contribute to age-related differences in plasma lipoprotein concentrations in men?

Age-related differences in body fat and more specifically in the accumulation of abdominal visceral adipose tissue were examined as a potential covariate for the alteration in the plasma lipoprotein profile found with aging. For that purpose, results from 79 young adults (aged 24.5 +/- 4.0 years) were compared to 61 middle-aged men (54.7 +/- 6.4 years). Younger men had significantly lower body fat mass and abdominal visceral adipose tissue area measured by computed tomography than middle-aged men (P < 0.0001). Plasma cholesterol, triglyceride, apolipoprotein (apo) B, low density lipoprotein (LDL)-cholesterol and LDL apo B levels, as well as the ratio of plasma cholesterol to high density lipoprotein (HDL)-cholesterol were all significantly lower in younger men as compared to middle-aged men (P < 0.0001). The comparison of younger men to middle-aged men with comparable levels of abdominal visceral fat and total body fat eliminated the age-related differences in plasma triglyceride and in the ratio of plasma cholesterol to HDL-cholesterol, whereas the difference in plasma apolipoprotein B levels, although still significant, was largely reduced. Age-related differences in plasma cholesterol and in LDL-cholesterol levels were still observed after this matching procedure and the differences between age-groups were essentially of similar magnitude than before pairing. In summary, these results suggest that the deterioration of plasma lipoprotein profile observed in middle-aged men as compared to young adult men is partly mediated by concomitant increases in total body fat and abdominal visceral adipose tissue. However, other factors related to the aging process appear to be involved, particularly for the age-related increase in plasma LDL-cholesterol.

Adipose Tissue↗

Does lipoprotein or hepatic lipase activity explain the protective lipoprotein profile of premenopausal women?

Numerous studies have reported that women have a lipoprotein profile suggestive of a reduced risk of coronary heart disease (CHD). We have therefore tested whether the "protective" lipoprotein profile of women could be explained by differences in hepatic lipase (HL) or lipoprotein lipase (LPL) activities. In the present study, 14 non-obese healthy premenopausal women had higher plasma concentrations of high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, and HDL-apolipoprotein (apo) AI, and a higher ratio of HDL-C to low-density lipoprotein cholesterol (LDL-C) than 17 non-obese healthy men. Women also had lower plasma triglyceride (TG), HDL-TG, and apo B levels than men. Plasma postheparin LPL (PH-LPL) and HL activities showed no significant sex dimorphism, whereas abdominal and femoral adipose tissue (AT)-LPL activities were significantly higher in women (P < .005). In men, PH-LPL activity correlated significantly with plasma HDL2-C (r = .52, P < .05), LDL-C (r = -.47, P < .05), and apo B (r = -.56, P < .01) levels, as well as with the HDL-C/LDL-C ratio (r = .67, P < .005). No such relationships were found in women, with the exception of HL activity, which was negatively correlated with HDL-apo AI levels. In both genders, abdominal AT-LPL activity showed no significant association with plasma lipoprotein levels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Reduced testosterone and adrenal C19 steroid levels in obese men.

It has been reported that a high proportion of abdominal fat is associated with increased plasma androgen concentrations in women. Although less evidence is available, abdominal obesity appears to be associated with low plasma testosterone (T) levels in men. We have therefore examined in 80 men (aged 36.3 +/- 3.2 years, mean +/- SD) the correlations between body fatness, adipose tissue (AT) distribution measured by computed tomography (CT), and circulating levels of the following steroids measured by radioimmunoassay after extraction from serum and chromatography: dehydroepiandrosterone (DHEA), androstenedione (delta 4-DIONE), androst-5-ene-3 beta,17 beta-diol (delta 5-DIOL), T, estrone, and estradiol. Sex hormone-binding globulin (SHBG) levels were also determined. T, adrenal C19 steroids, and SHBG levels were negatively correlated with total body fatness indices and abdominal fat deposition measured by CT (-.23 < or = -.55, .0001 < or = P < or = .05), whereas estrone showed positive correlations with these body fatness and AT distribution indices. Covariance analysis showed that after control for the concentration of the adrenal steroid precursor delta 5-DIOL, there was no residual association between T levels and adiposity variables. Furthermore, multivariate analyses showed that steroid and SHBG levels could explain from 20% (visceral AT area measured by CT) to 40% and 42% (body mass index [BMI], waist circumference, and waist to hip ratio [WHR]) of the variation in adiposity variables (.0001 < or = P < or = .05), with delta 5-DIOL being the best single correlate of body fatness and abdominal fat deposition in men.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

The lipoprotein lipase HindIII polymorphism modulates plasma triglyceride levels in visceral obesity.

The aim of this study was to investigate the potential interaction between the lipoprotein lipase (LPL) HindIII polymorphism and visceral adipose tissue (AT) accumulation in the modulation of triglyceride levels in visceral obesity. The LPL-HindIII genotype was determined by polymerase chain reaction in 52 min. Twenty-three subjects were heterozygous (+/-) and 28 were homozygous (+/+) for the presence of the restriction site. One subject who was homozygous for the--allele was excluded from analysis. Body mass index (BMI), fasting insulin level, and visceral AT area as measured by computed tomography were positively correlated with triglyceride levels only in subjects homozygous for the + allele. Furthermore, whereas these variables were negatively correlated with plasma HDL2 cholesterol concentrations in the +/+ group, these associations were not found in +/- heterozygotes, with the exception of BMI. To further investigate the interaction of the LPL-HindIII polymorphism with visceral obesity and hyperinsulinemia, the two genotype groups were further subdivided on the basis of BMI (low versus high), fasting insulin level (low versus high), and visceral AT area (low versus high), and their lipoprotein profiles were compared. Elevated levels of abdominal visceral AT were significantly associated with increased triglyceride concentrations in +/+ homozygous men, suggesting that visceral obesity may lead to hypertriglyceridemia in the presence of the +/+ genotype. In the +/- group, variation in the amount of visceral AT was not associated with differences in triglyceride concentration. However, hypertriglyceridemia and an increased cholesterol-to-HDL cholesterol ratio were observed in the hyperinsulinemic state irrespective of LPL-HindIII genotype status.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Relation of steroid hormones to glucose tolerance and plasma insulin levels in men. Importance of visceral adipose tissue.

OBJECTIVE: Low plasma testosterone levels are associated with hyperinsulinemia and glucose intolerance in men. However, it is unclear whether these abnormalities are related to the concomitant alteration in regional adipose tissue (AT) accumulation associated with reduced androgen levels. RESEARCH DESIGN AND METHODS: We measured plasma steroid levels in a sample of 79 men, ranging from lean to obese (aged 29-42 years), for whom an oral glucose tolerance test (OGTT), anthropometric and computed tomography (CT) measurements of body fatness, and AT distribution were performed. Sex hormone binding globulin (SHBG) and the following steroids were measured after extraction from plasma and chromatography: dehydroepiandrosterone, androstenedione, androst-5-ene-3 beta,17 beta-diol, testosterone, estrone, and estradiol (E2). RESULTS: Several significant negative correlations were found between adrenal C19 steroid precursors, testosterone, SHBG, and fasting insulin levels, as well as between plasma glucose and insulin concentrations measured during the OGTT (-0.25 < or = r < or = -0.35, 0.05 > or = P > or = 0.001). The best steroid correlate of plasma glucose and insulin homeostasis indexes was the E2: testosterone ratio (0.34 < or = r < or = 0.42, 0.005 > or = P > or = 0.001). However, after correction of steroid levels for either fat mass, body mass index (BMI), or visceral AT area, as measured by CT, no significant residual associations were noted between testosterone, adrenal C19 steroid, SHBG, and estrogen levels and indexes of plasma glucose-insulin homeostasis, although the positive association between the E2: testosterone ratio and glucose area remained significant after adjustment for total body fat mass and BMI. Furthermore, 15 pairs of obese subjects, matched for visceral AT area, showing either low or high levels of the steroids studied, did not differ in fasting insulin and postglucose plasma insulin levels or in glucose tolerance. CONCLUSIONS: These results suggest that the previously reported relationships between androgen levels and indexes of plasma glucose-insulin homeostasis are mediated, to a large extent, by concomitant alterations in levels of total body fat and visceral AT in men.

Adipose Tissue↗

Role of dietary fish protein in the regulation of plasma lipids.

The following studies have been carried out to compare the effects of fish protein with other dietary proteins on plasma cholesterol and lipoproteins in animal models and in humans. In rabbits, fish protein has been shown to induce relatively variable effects compared to casein and soy protein on serum cholesterol depending in part on the origin of dietary lipids with which it is combined. In a protein-lipid interaction study, casein, soy or cod protein were combined with corn or coconut oil. Casein and soy protein in the presence of corn oil induced lower serum cholesterol levels despite its combination with either corn or coconut oil. This is in part due to serum high density lipoprotein (HDL) cholesterol concentrations, which were consistently higher with cod protein than with either casein or soy protein, regardless of the dietary lipid source. In rabbits, this rise in HDL cholesterol was associated with a decrease in very low density lipoprotein (VLDL) triglycerides and an increase in postheparin plasma lipoprotein lipase activity. The effects of lean white fish on plasma lipoproteins also have been investigated in post and premenopausal women fed a low-fat, high P/S (polyunsaturated/saturated fat) ratio diet. In postmenopausal women, lean white fish compared with other animal protein products induced higher concentrations of plasma cholesterol, LDL-apolipoprotein (apo) B and HDL cholesterol, mainly in the HDL3 fraction. In premenopausal women, lean white fish induced lower concentrations of VLDL triglycerides and higher concentrations of LDL-apoB in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗