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At least 433 records · Page 24Linked to original sources
PubMed1995

Coordinated regulation of hormone-sensitive lipase and lipoprotein lipase in human adipose tissue in vivo: implications for the control of fat storage and fat mobilization.

The enzymes lipoprotein lipase (LPL, EC 3.1.1.34) and hormone-sensitive lipase (HSL, EC 3.1.1.3) apparently catalyze opposing functions in white adipose tissue: the former is concerned with fat storage, the latter with fat mobilization. We have studied their regulation in vivo in normal subjects in the postabsorptive state and after eating meals of different compositions, by measurement of arteriovenous concentration differences for triacylglycerol, non-esterified fatty acids and glycerol across a subcutaneous adipose depot. The two enzymes are regulated in a broadly reciprocal manner: in the overnight-fasted state, HSL is more active, but after a meal HSL is suppressed whilst LPL is activated. The movement of fatty acids in and out of adipose tissue appears to be driven by concentration gradients generated by regulation of these two enzymes, and also by activation, in the postprandial period, of the process of fatty acid esterification. The results show some interesting and perhaps unexpected features of metabolic regulation. Of the fatty acids generated by the action of LPL on circulating TAG, a large proportion is released directly into the venous plasma: close to 100% in the overnight-fasted state, and 50% or more at the peak of LPL action after a meal, making what appear reasonable assumptions. We suggest that this apparent 'inefficiency' of fat storage reflects the energetic cost of maintaining precise control over such a fundamental process. Although LPL is usually thought of as the enzyme regulating fat deposition, in fact the fatty acids and glycerol it releases from circulating TAG represent a substantial proportion of those released from adipose tissue, especially in the postprandial state. In addition, although HSL is considered the enzyme responsible for fat mobilization, suppression of its activity is essential to normal regulation of fat deposition. Thus, fat storage and fat mobilization during normal daily life are controlled by coordinated regulation of a number of enzymatic processes in white adipose tissue.

Adipose Tissue↗
PubMed1994

Eating fat or being fat and risk of cardiovascular disease and cancer among women.

This article first reviews the relationship between intake of saturated fat and cholesterol and atherosclerosis; then the relationship between fat intake, obesity, and disease; and finally, some of the determinants of obesity and weight gain. The percentage of saturated fat and cholesterol in the diet is the major determinant of atherosclerosis and coronary heart disease among populations. In addition, fat intake is directly related to obesity. The degree of obesity is a major determinant of blood glucose and insulin, high-density-lipoprotein cholesterol, and triglycerides. Weight gain, especially after adolescence, and high fat intake may contribute, to a greater extent, to metabolically active intra-abdominal fat and risk of disease. Fat in diet, weight gain, or obesity may play an important role in sex-steroid hormone metabolism. Hormonal changes may contribute to an increased risk of breast cancer. The risks associated with eating fat may be related to the time of development of obesity (i.e., weight gain) and the balance between effects on sex-steroid hormone metabolism and insulin-glucose metabolism.

Arteriosclerosis↗
PubMed2005

Novel approach on the risk assessment of oxidized fats and oils for perspectives of food safety and quality. I. Oxidized fats and oils induces neurotoxicity relating pica behavior and hypoactivity.

Food poisoning caused by deteriorated fat and oil in instant noodles was first reported in Japan approximately 40 years ago. In these cases, many people developed neurotoxic symptoms such as emesis and discomfort. The degree of oxidation of the fat and oil in the instant noodles that induced food poisoning was at least 100 meq/kg in peroxide value (PV). No general toxicity studies with animals, however, have examined the toxicity of fat and oil oxidized to that extent. In this study, pica behavior, a behavior characterized by eating a nonfood material such as kaolin and that relates to the degree of discomfort in animals, and alterations of locomotor activity of rats eating deteriorated fat and oil were measured. The groups fed fat and oil with at least 138.5 meq/kg PV consumed significantly more kaolin compared to the control group. Furthermore, rats that ate deteriorated fat and oil with at least 107.2 meq/kg PV had significantly decreased locomotor activity compared to control rats. These phenomena suggest that oxidized fat and oil with at least 100 meq/kg PV induce neurotoxicity. The toxicity of oxidized fat and oil has only been addressed using general toxicity tests, but the present results reveal the importance of evaluating toxicity by using other measures.

Animals↗
PubMed2003

Green tea reduces body fat accretion caused by high-fat diet in rats through beta-adrenoceptor activation of thermogenesis in brown adipose tissue.

The aim of the present study was to investigate body fat-suppressive effects of green tea in rats fed on a high-fat diet and to determine whether the effect is associated with beta-adrenoceptor activation of thermogenesis in brown adipose tissue. Feeding a high-fat diet containing water extract of green tea at the concentration of 20g/kg diet prevented the increase in body fat gain caused by high-fat diet without affecting energy intake. Energy expenditure was increased by green tea extract which was associated with an increase in protein content of interscapular brown adipose tissue. The simultaneous administration of the beta-adrenoceptor antagonist propranolol(500 mg/kg diet) inhibited the body fat-suppressive effect of green tea extract. Propranolol also prevented the increase in protein content of interscapular brown adipose tissue caused by green tea extract. Digestibility was slightly reduced by green tea extract and this effect was not affected by propranolol. Therefore it appeared that green tea exerts potent body fat-suppressive effects in rats fed on a high-fat diet and the effect was resulted in part from reduction in digestibility and to much greater extent from increase in brown adipose tissue thermogenesis through beta-adrenoceptor activation.

Adipose Tissue↗
PubMed2005

NO-1886 (ibrolipim), a lipoprotein lipase activator, increases the expression of uncoupling protein 3 in skeletal muscle and suppresses fat accumulation in high-fat diet-induced obesity in rats.

Although the lipoprotein lipase (LPL) activator NO-1886 shows antiobesity effects in high-fat-induced obese animals, the mechanism remains unclear. To clarify the mechanism, we studied the effects of NO-1886 on the expression of uncoupling protein (UCP) 1, UCP2, and UCP3 in rats. NO-1886 was mixed with a high-fat chow to supply a dose of 100 mg/kg to 8-month-old male Sprague-Dawley rats. The animals were fed the high-fat chow for 8 weeks. At the end of the administration period, brown adipose tissue (BAT), mesenteric fat, and soleus muscle were collected and levels of UCP1, UCP2, and UCP3 messenger RNA (mRNA) were determined. NO-1886 suppressed the body weight increase seen in the high-fat control group after the 8-week administration (585 +/- 39 vs 657 +/- 66 g, P < .05). NO-1886 also suppressed fat accumulation in visceral (46.9 +/- 10.4 vs 73.7 +/- 14.5 g, P < .01) and subcutaneous (43.1 +/- 18.1 vs 68.9 +/- 18.8 g, P < .05) tissues and increased the levels of plasma total cholesterol and high-density lipoprotein cholesterol in comparison to the high-fat control group. In contrast, NO-1886 decreased the levels of plasma triglycerides, nonesterified free fatty acid, glucose, and insulin. NO-1886 increased LPL activity in soleus muscle (0.082 +/- 0.013 vs 0.061 +/- 0.016 mumol of free fatty acid per minute per gram of tissue, P < .05). NO-1886 increased the expression of UCP3 mRNA in soleus muscle 3.14-fold (P < .01) compared with the high-fat control group without affecting the levels of UCP3 in mesenteric adipose tissue and BAT. In addition, NO-1886 did not affect the expression of UCP1 and UCP2 in BAT, mesenteric adipose tissue, and soleus muscle. In conclusion, NO-1886 increased the expression of UCP3 mRNA and LPL activity only in skeletal muscle. Therefore, a possible mechanism for NO-1886's antiobesity effects in rats may be the enhancement of LPL activity in skeletal muscle and the accompanying increase in UCP3 expression.

Adipose Tissue↗
PubMed1997

Fat preferences, dietary fat intake and body composition in children.

OBJECTIVE: To examine the relationship between fat preference, dietary intake data and body composition in children. SUBJECT AND METHODS: Subjects studied were 88 children aged 9-12 y from two elementary schools in Ohio. Measures for dietary intake and body composition were obtained by 3 day diet records, anthropometrics, triceps and subscapular skinfolds. Fat preference data was assessed by hedonic rating of high and low fat snack foods. RESULTS: Data indicate that children who preferred the high fat snack items had high dietary fat intakes (r = 0.57, P < 0.05). Tricep skinfold measurement and BMI correlated positively with high fat food preferences (r = 0.51 and r = 0.46 P < 0.05). CONCLUSIONS: These data suggest preference for high fat foods may occur due to diet composition and that increased adiposity may be associated with higher relative fat intakes.

Body Composition↗
PubMed1998

The high-fat phenotype: is leptin involved in the adaptive response to a high fat (high energy) diet?

OBJECTIVE: To investigate physiological differences which could influence the balance between energy expenditure and energy intake, between habitual high-fat (HF) and low-fat (LF) consumers and the potential for weight gain. SUBJECTS: Ten HF and nine LF consumers, all young, lean males (% energy from fat 45.4 and 31.8, respectively). MEASUREMENTS: Habitual dietary variables (from the food frequency questionnaire, FFQ), body mass index (BMI), % body fat (% BF, measured by impedance), fasting concentrations of plasma leptin, glucose and triglycerides. RESULTS: HF and LF subjects (selected for their fat intake) did not differ significantly in BMI or % BF. HF subjects had significantly higher concentrations of plasma leptin and lower concentrations of plasma glucose than LF subjects. In all subjects, concentrations of fasting plasma leptin correlated significantly with BMI, % BF and fat mass; difference in leptin between groups remained significant when BMI and % BF were used as covariants. Leptin significantly correlated with dietary variables; particularly dietary fat (% energy and g) and inversely with dietary carbohydrate (% energy), but showed no correlation with dietary protein or total energy intake. CONCLUSION: Significant differences in concentrations of fasting plasma leptin have been observed between lean male HF and LF consumers. These findings suggest that the difference in leptin concentrations could be associated with a metabolic adaptation which could help to offset the weight inducing properties of high fat (high energy) diets.

Adaptation, Physiological↗
PubMed1999

Reduction in fat storage during chitin-chitosan treatment in mice fed a high-fat diet.

OBJECTIVE: Chitin and chitosan are polymers containing more than 5000 acetylglucosamine and glucosamine units, respectively, and their molecular weights are over one million Daltons. The present study assessed the effects of chitin-chitosan on the activity of pancreatic lipase in vitro and on the degree of fat storage induced in mice by the oral administration of a high-fat diet for nine weeks. DESIGN: Mice were fed a high-fat diet and treated with chitin-chitosan for nine weeks. Experiments were also carried out to clarify whether or not chitin-chitosan inhibited pancreatic lipase activity in assay systems using triolein emulsified with lecithin, gum arabic or Triton X-100. RESULTS: Chitin-chitosan prevented the increase of body weight, hyperlipidaemia and fatty liver induced by a high-fat diet. Chitin-chitosan inhibited hydrolysis of triolein, emulsified with phosphatidylcholine, but not that of triolein emulsified with gum arabic and Triton X-100. These results suggest that the site of inhibitory action of chitin-chitosan may not be the enzyme but its substrate. CONCLUSION: The anti-obesity effects of chitin-chitosan in high-fat diet-treated mice might be partly due to the inhibition of intestinal absorption of dietary fat. Consequently, chitin-chitosan might cause improvement of the fatty liver and hyperlipidaemia in mice fed a high fat diet through inhibiting intestinal absorption of dietary fat.

Adipose Tissue↗
PubMed2004

Effects of structured medium- and long-chain triacylglycerols in diets with various levels of fat on body fat accumulation in rats.

The effects of structured medium- and long-chain triacylglycerols (MLCT) in diets containing 50-200 g fat/kg on body fat accumulation were compared with those of long-chain triacylglycerols (LCT) in rats. In rats fed ad libitum, weights of intra-abdominal adipose tissues and carcass fat contents were significantly smaller (P<0.05) in rats fed the 150-200 g MLCT/kg diet than in rats fed 150-200 g LCT/kg diet. Serum and liver triacylglycerol contents were significantly greater (P<0.05) in rats fed 200 g MLCT/kg diet, as were hepatic capacities of citrate synthase and cytochrome oxidase (P<0.05). The effects of MLCT on body fat were also examined in adult rats fed a limited amount of food (approximately 50 % of ad libitum intake). Reduction of body fat deposition during the food restriction was the same between in LCT and MLCT groups. These results suggest that accumulation of body fat was less efficient during long-term feeding of MLCT than LCT in rats fed high-fat diets ad libitum. The effect of MLCT on body fat might be influenced by the dietary fat content or by energy sufficiency.

Adipose Tissue↗
PubMedDate not supplied

[Nutritive physiological effect of dietary fats in rations for growing swine. 2. Effect of an isocaloric exchange of carbohydrate energy versus fat energy in piglets on growth and various metabolic parameters in the subsequent fattening period].

The influence of different feeding regimes of piglets on fattening performance and blood composition of the subsequent fattening period (30-100 kg) was examined. Three groups of pigs fed on an isocaloric and isonitrogenous basis with rations containing either 5% fat (groups I), 18% fat (group II) or 35% fat (group III) until body weight of 30 kg, were fed ad libitum one diet from 30 kg onwards. At a body weight of 45 and 93 kg the blood concentrations of insulin, glucose, urea, free fatty acids, neutral lipids and cholesterol in response to feeding and of insulin and glucose in response to an oral glucose load was determined in pigs provided with a permanent jugular vein catheter. Moreover, the in-vitro fat synthesis from glucose was measured. At the end of the experiment the body composition was determined by chemical analysis of the carcass. Neither feed intake, daily body weight gain nor feed conversion differed significantly among the groups. Blood urea levels of the three groups did not suggest a different protein utilization. Neither feed consumption nor oral intake of glucose affected the insulin and glucose response of the three groups differently. The concentrations of free fatty acids, neutral lipids and cholesterol did not differ clearly among the groups although occasionally significance of difference was observed. In group I the in-vitro synthesis of fat was increased (p less than 0.05) at a body weight of 45 kg and appeared to be higher at a body weight of 93 kg as compared to the high fat group (group III). No clear differences between the groups were observed in the chemical composition of the carcasses. It is concluded, that isocaloric replacement of carbohydrates by fat in the diet of piglets does not affect protein and fat retention in the subsequent fattening period.

Animals↗
PubMed1993

Dietary fat and the control of energy intake: evaluating the effects of fat on meal size and postmeal satiety.

Three separate experiments in lean subjects confirmed that a 1.52-MJ (362-kcal) carbohydrate supplement at breakfast suppressed appetite 90 min later but had no effect on a test meal given after 270 min. A 1.52-MJ (362-kcal) fat supplement produced no detectable action on measures of appetite at any time point. Therefore, fat and carbohydrate do not have identical effects on the appetite profile. In a further study in obese subjects, a novel experimental design was used to assess the satiating efficiency and compensatory response of fat. Eating from a range of either high-fat or high-carbohydrate foods, obese subjects voluntarily consumed twice as much energy from the fat items, thereby indicating a weak action of fat on satiation. In turn, this large intake of fat exerted a disproportionately weak effect on satiety. These studies suggest that the appetite-control system may have only weak inhibitory mechanisms to prevent the passive overconsumption of dietary fat. The results indicate how this action could induce a positive energy balance and lead to a gradual upward drift in body mass index.

Analysis of Variance↗
PubMed2000

Fat intake and breast cancer risk in an area where fat intake is low: a case-control study in Indonesia.

BACKGROUND: Associations of fat and other macronutrients with breast cancer risk are not clear in areas where fat intake is low. METHODS: We conducted a hospital-based case-control study from 1992 to 1995 in Jakarta, Indonesia. RESULTS: The study, based on 226 cases and 452 age and socioeconomic status matched controls, provided the following findings. (a) In the pre-marriage period, the greater the fat or protein consumption, the larger the risk, whereas decreasing risk with increasing carbohydrate intake was detected. The odds ratio (OR) for the highest quartile of intake relative to the lowest was 8.47 (95% CI: 4.03-17.8) for fat, 2.19 (95% CI: 1.30-3.69) for protein, and 0.16 (95% CI: 0.08-0.31) for carbohydrate. A positive association with fat and a negative one with carbohydrate were also observed for the post-marriage period, but of weaker magnitude compared to the pre-marriage period. (b) The effects of macronutrient intakes were stronger among premenopausal than among postmenopausal women. (c) Most of the associations of protein and carbohydrate were insignificant after adjustment for fat intake. CONCLUSIONS: These findings suggest that fat intake might be an important determinant of breast cancer among populations with a low fat diet in Indonesia.

Adult↗
PubMed1977

Fatty acid synthesis in testes of fat-deficient and fat-supplemented rats.

Fatty acid synthesis was studied in testes of rats fed a fat-free or fat-supplemented diet. Testes of fat-deficient rats incorporated nearly twice as much intratesticularly injected [1-14C]acetate into total fatty acids (primarily into palmitic acid) as did supplemented rats. To determine the mechanism for the increased synthesis, the activities of the following enzymes were determined in the cytoplasmic fraction of testicular homogenates: fatty acid synthetase, acetyl CoA carboxylase [EC 6.4.1.2], citrate-cleavage [EC 4.1.3.8], malic [EC 1.1.1.38], and the glucose-l-phosphate dehydrogenase [EC 1.1.1.49]: 6-phosphogluconate dehydrogenase pair [EC 1.1.1.44]. Although the activity of fatty acid synthetase did increase in livers from fat-deficient rats, no change was observed in corresponding testes. No difference between the two groups could be demonstrated in testicular activity of citrate-cleavage enzyme, malic enzyme, or the glucose-6-phosphate dehydrogenase: 6-phosphogluconate dehydrogenase pair. However, the activity of cytoplasmic acetyl CoA carboxylase in testes of rats fed the fat-deficient diet was 1.4 times higher than the activity in testes of rats fed the supplemented diet. Fat deficiency did not affect the specific activity of the testicular microsomal elongation system, assayed by incubation with 14C-malonyl CoA. The concentration of unesterified fatty acids was lower in testes of the fat-deficient compared to supplemented rats, indicating that decreased inhibition of acetyl CoA carboxylase in the fat-deficient rats testes might have been responsible for the observed increased de novo synthesis of palmitic acid.

ATP Citrate (pro-S)-Lyase↗
PubMed1992

Plasma esterase-1 (ES-1) activity in rats is influenced by the amount and type of dietary fat, and butyryl cholinesterase activity by the type of dietary fat.

In previous work, we studied, under conditions of ad libitum food consumption, the effect of amount and type of dietary fat on plasma esterase-1 (ES-1) and butyryl cholinesterase activity in rats. This was done by the isoenergetic replacement of dietary fat by carbohydrates or by another fat source. The observed change in enzyme activity could theoretically be determined by either the dietary omission or the addition or by the combination. In the present work, we studied under restricted feeding conditions the effect of supplemental energy in various forms to determine the effect of the supplement alone. Supplemental coconut fat, but not isoenergetic amounts of either glucose or casein, raised plasma ES-1 activity. None of these supplements influenced butyryl cholinesterase activity. In a second experiment, we demonstrated that the ES-1 enhancing effect of supplemental coconut fat also occurred with fish oil, whereas the stimulatory effects of olive oil and corn oil were less pronounced. Supplemental fish oil, but not the three other fats, significantly reduced the depression in butyryl cholinesterase activity. Plasma cholesterol concentration was negatively associated with butyryl cholinesterase activity, but was not related to ES-1 activity. The two esterases were not correlated with plasma triglyceride concentration. We conclude that both the amount and type of fat in the diet of rats have specific influences on plasma ES-1 activity and that butyryl cholinesterase activity is affected by the type of fat.

Animal Feed↗
PubMed1999

Left ventricular mass correlates with fat-free mass but not fat mass in adults.

BACKGROUND: Left ventricular mass is associated with body size, obesity and blood pressure. Echocardiography is routinely used to estimate this parameter, which is usually indexed to body surface area to allow comparisons to be made between individuals and groups of different body size. However, in obese subjects, using left ventricular mass indexed to body surface area may inappropriately normalize left ventricular mass. OBJECTIVES: The aim of this study was to investigate the relationships between left ventricular mass and body composition and to determine the best determinants of left ventricular mass. SUBJECTS AND METHODS: Echocardiography and dual-energy X-ray absorptiometry were performed in 106 subjects under primary care. Half were hypertensive subjects and the others were normotensive age- and sex-matched control subjects. Univariate correlations were studied between left ventricular mass and height, height1.5, height2.7, weight, body surface area, body mass index, waist: hip ratio, fat-free mass, bone mineral content and fat mass. Stepwise multiple linear regression was performed to determine the best determinants of left ventricular mass. RESULTS: Fat-free mass was correlated with left ventricular mass (r = 0.53, P = 0.0001) and was the only independent predictor of left ventricular mass (R2 = 0.30, P= 0.0001) by multivariate analysis. Fat mass did not correlate with left ventricular mass (r= -0.005, P= 0.96). Other measures of body size, including body surface area, waist: hip ratio, bone mineral content, weight, height, height 1.5, height2.7 and body mass index all were correlated with, but were not independent determinants of, left ventricular mass. CONCLUSIONS: Left ventricular mass is independently determined by fat-free mass but by no other measures of body size or composition. Specifically, left ventricular mass was neither correlated with nor determined by fat mass. None of the other measures of body size determined left ventricular mass. It may be more appropriate to index left ventricular mass to fat-free mass rather than to measures of body size which include fat mass.

Aged↗
PubMed2006

Assessment of the risk of systemic fat mobilization and fat embolism as a consequence of liposuction: ex vivo study.

BACKGROUND: Adverse consequences of liposuction, including those associated with fat embolism, have been reported in the literature. Fat embolism syndrome after liposuction may be underestimated because of the unspecific nature of the symptoms. The aim of this study was to determine whether there is a generic risk of the generation of intravascular fat emboli as a consequence of liposuction. METHODS: An animal study was conducted in which liposuction was performed on 10 Sprague-Dawley rats. The procedure was conducted with the animals under general anesthesia for 60 minutes, in a similar manner to that practiced clinically. Three blood samples were taken from each animal through a central line (one before liposuction and two at 30 and 60 minutes into liposuction) and examined for the presence of fat particles. The animals were then euthanized and the lungs and brain were removed for histological examination. In the control group, liposuction was not performed, but similar blood and histological samples were taken. RESULTS: In the study group, stained fat particles were seen in all blood samples taken during liposuction but not in those taken before liposuction. The difference between the 30- and 60-minute samples and the preliposuction control ones was statistically significant (p < 0.001 minimum). The differences between the 30-minute and 60-minute samples were also statistically significant (p = 0.017), demonstrating that fat mobilization during liposuction is a cumulative process. Nothing of significance was seen in the blood samples of the control group. Lipid deposits were seen in the lungs of all study group animals but not in the control group. With one possible exception, no lipid deposits were confirmed in brain specimens. CONCLUSIONS: The authors' experiments have demonstrated a significant risk of systemic fat mobilization and fat embolism after liposuction in the animal model. Further clinical investigation is required to evaluate the real clinical risk of this procedure from this perspective.

Animals↗
PubMed1992

Effects of switching from a high-fat diet to a low-fat diet on tumor proliferation and cell kinetics of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma in rats.

We investigated the stimulatory effect of a high-fat diet on tumorigenesis, tumor proliferation and cell kinetics of 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas in Sprague-Dawley rats, and sought to determine whether switching the animals from a high-fat diet to a low-fat diet would suppress tumor proliferation and cell kinetics. The high-fat diet significantly stimulated tumorigenesis, tumor proliferation and cell kinetics. After the animals were switched from the high-fat diet to the low-fat diet, however, tumor growth decreased, the BrdUrd labeling indices of tumors significantly decreased, and the potential doubling times of tumors significantly increased. Therefore, switching from a high-fat diet to a low-fat diet may improve the prognosis of breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Body fat distribution is a determinant of the high-density lipoprotein response to dietary fat and cholesterol in women.

We have conducted a dietary trial that addressed the factors influencing the variability in plasma lipids in response to dietary fat and cholesterol with a focus on the effects of gender and body fat distribution. Sixty-seven women and 53 men were selected so that overall men and women had a similar mean age, LDL cholesterol, and body mass index. After a 2-week low-fat period subjects were given two liquid supplements for 3 weeks each, one that contained 31 to 40 g fat and 650 to 845 mg cholesterol, and one that was fat free. Measurements included plasma lipids and lipoproteins, glucose, insulin, hepatic triglyceride lipase activity, apolipoprotein E polymorphism, and three indexes of body fat (body mass index, waist girth, and waist-hip ratio). In response to dietary fat and cholesterol supplementation only the changes in HDL cholesterol, especially in HDL2, differed between the sexes. Although on univariate analysis lipoprotein changes were predicted by baseline lipoprotein levels, body mass index, waist girth, waist-hip ratio, hepatic triglyceride lipase activity, and insulin, multiple regression showed only waist-hip ratio to predict changes in HDL2 cholesterol in women and body mass index and baseline HDL2 cholesterol in men. Changes in LDL were predicted by baseline LDL cholesterol in women and apolipoprotein E phenotype and age in men. These studies explain much of the variability that individuals show in lipoprotein changes, especially in the more desirable changes in cholesterol transport in HDL2, in response to eating saturated fat and cholesterol.

Adipose Tissue↗