Dietary cholesterol and the plasma lipids and lipoproteins in the Tarahumara Indians: a people habituated to a low cholesterol diet after weaning

1. The effects of feeding isolated saponins on plasma lipid concentrations and on concentrations of biliary and faecal bile acids and neutral sterols were studied in the rat.2. The animals were given one of four diets, i.e. a standard low-cholesterol synthetic diet, the diet+10 g saponins/kg, the diet+10 g cholesterol/kg, the diet+10 g cholesterol+10 g saponins/kg.3. Saponins partially reversed the hypercholesterolaemia caused by the high-cholesterol diet and increased both the rate of bile acid secretion and the faecal excretion of bile acids and neutral sterols. The proportionate contribution of the primary bile acids (particularly chenodeoxycholic) to faecal excretion was also increased by saponins.4. The results are discussed in relation to the hypothesis that saponins act by inducing the adsorption of bile acids by dietary fibre.

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Prospective, Randomized, Infancy-Onset Trial of the Effects of a Low-Saturated-Fat, Low-Cholesterol Diet on Serum Lipids and Lipoproteins Before School Age

Circulation ◽

10.1161/01.cir.102.13.1477 ◽

2000 ◽

Vol 102 (13) ◽

pp. 1477-1483 ◽

Cited By ~ 35

Author(s):

Leena Rask-Nissilä ◽

Eero Jokinen ◽

Tapani Rönnemaa ◽

Jorma Viikari ◽

Anne Tammi ◽

...

Keyword(s):

Serum Lipids ◽

Saturated Fat ◽

School Age ◽

Cholesterol Diet ◽

Before School ◽

Lipids And Lipoproteins ◽

Low Cholesterol

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Efficacy of Ganoderma lucidum on plasma lipids and lipoproteins in rats fed with high cholesterol diet

Nutrition & Food Science ◽

10.1108/00346650810871911 ◽

2008 ◽

Vol 38 (3) ◽

pp. 229-238 ◽

Cited By ~ 3

Author(s):

Chow‐Chin Tong ◽

Yew‐Keong Choong ◽

Suhaila Mohamed ◽

Noordin Mohamed Mustapha ◽

Nor Aini Umar

Keyword(s):

Ganoderma Lucidum ◽

Plasma Lipids ◽

High Cholesterol Diet ◽

Cholesterol Diet ◽

High Cholesterol ◽

Lipids And Lipoproteins

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Relation of dietary cholesterol and fat to atheromatosis in laying and nonlaying hens

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.1.71 ◽

1961 ◽

Vol 200 (1) ◽

pp. 71-74 ◽

Cited By ~ 1

Author(s):

A. C. Ivy ◽

C. S. N. Setty ◽

R. Suzuki

Keyword(s):

High Fat Diet ◽

Dietary Cholesterol ◽

Relative Energy ◽

Egg Laying ◽

The Other ◽

Cholesterol Diet ◽

High Fat ◽

One Year ◽

Low Cholesterol ◽

Rate Of Accumulation

Twenty-four female chicks received a diet containing 0.05% cholesterol, 3% fat and 22% protein for 6 months. Then, 12 of them, 6 good layers and 6 non- or poor layers, received a diet containing 0.03% cholesterol, 2.4% fat and 14.25% protein for 52 weeks. The other 12 received a diet containing 0.08% cholesterol, 7% fat (6.5 gm/100 gm of diet being beef tallow, m.p. 42°C) and 17.44% protein, the relative energy values being 774 and 1001 calories, respectively. These diets were fed 12 months, at the end of which period the chickens were 18 months of age. In the 12 hens on the ‘low-fat, low-cholesterol’ diet, the incidence and severity of atheromatosis was 25% and 5%, respectively; in the 12 on the ‘high-fat’ diet it was 75% and 25%, respectively. There was no difference in the incidence and severity of atheromatosis between the ‘layers’ and ‘nonlayers.’ Since egg laying is associated with a marked hyperlipemia and not a hypercholesterolemia, these results show also that a hyperlipemia alone though present for almost one year does not increase the rate of accumulation of cholesterol in the arteries of hens.

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Interrelationships between Nutrient Intake and Plasma Lipids and Lipoproteins in Schoolchildren Aged 6 to 19: The Princeton School District Study

PEDIATRICS ◽

10.1542/peds.65.4.727 ◽

1980 ◽

Vol 65 (4) ◽

pp. 727-734

Author(s):

John A. Morrison ◽

Rhea Larsen ◽

Lenora Glatfelter ◽

Donna Boggs ◽

Kathryn Burton ◽

...

Keyword(s):

Nutrient Intake ◽

Plasma Lipids ◽

Plasma Cholesterol ◽

Dietary Cholesterol ◽

Saturated Fat ◽

Density Lipoprotein ◽

Lipoprotein Cholesterol ◽

Sucrose Intake ◽

Total Carbohydrate ◽

Lipids And Lipoproteins

Relationships between nutrient intakes and plasma lipids and lipoproteins were studied in 1,669 schoolchildren, aged 6 to 19 years; 948 were selected by random recall and 721 because of elevated plasma cholesterol or triglyceride (hyperlipidemic recall). Nutrient intake data was collected by using a 24-hour dietary recall. Median dietary cholesterol intakes for 6 to 9-year-old boys and girls in the random recall group were 222 and 230 mg/day, with polyunsaturated/saturated fat ratios of 0.34 and 0.33. For boys and girls, aged 10 to 12 years, median dietary cholesterol intakes were 296 and 235 mg/day, for 13 to 15 year olds, 343 and 237, and for 16 to 19 year olds, 418 and 221 mg/day. The dietary polyunsaturated/saturated fat ratios did not change appreciably with age. Partial correlation coefficients describing relationships between lipids, lipoproteins, and nutrients after adjustment for age, sex, race, and Quetelet index (W/H2) were calculated for all children (random and hyperlipidemic recall) after excluding children having plasma cholesterol, triglycerides, and calories less than or equal to the first or greater than or equal to the 99th percentiles for the random recall children. Plasma cholesterol was inversely and triglyceride positively correlated with dietary sucrose. Plasma low density lipoprotein cholesterol was inversely correlated with the dietary polyunsaturated/saturated fat ratio, total carbohydrate, and sugar. Potential relationships between nutrients and lipids-lipoproteins were also examined in children having low (first to tenth percentile), intermediate (45th to 55th percentile), and high (90th to 99th percentile) nutrient intake, after covariance adjustment for age, race, sex, and Quetelet index. Total plasma cholesterol fell as sucrose intake increased. Triglyceride rose along with caloric intake, total carbohydrate intake, and sucrose intake, while high density lipoprotein cholesterol levels fell with increasing caloric and sucrose intake. As dietary polyun-saturate ingestion rose from low to intermediate to high, plasma low density lipoprotein cholesterol increased. Nutrient intake may play a small but significant role relative to lipids and lipoproteins in children and, as such, may have importance relative to pediatric precursors of atherosclerosis.

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Mutants of the white ABCG Transporter in Drosophila melanogaster Have Deficient Olfactory Learning and Cholesterol Homeostasis

International Journal of Molecular Sciences ◽

10.3390/ijms222312967 ◽

2021 ◽

Vol 22 (23) ◽

pp. 12967

Author(s):

Jennifer L. Myers ◽

Maria Porter ◽

Nicholas Narwold ◽

Krishna Bhat ◽

Brigitte Dauwalder ◽

...

Keyword(s):

Cholesterol Efflux ◽

Dietary Cholesterol ◽

Olfactory Learning ◽

Cholesterol Homeostasis ◽

Cholesterol Diet ◽

Olfactory Conditioning ◽

Olfactory Memory ◽

Conditioning Paradigm ◽

Visual Defects ◽

Low Cholesterol

Drosophila’s white gene encodes an ATP-binding cassette G-subfamily (ABCG) half-transporter. White is closely related to mammalian ABCG family members that function in cholesterol efflux. Mutants of white have several behavioral phenotypes that are independent of visual defects. This study characterizes a novel defect of white mutants in the acquisition of olfactory memory using the aversive olfactory conditioning paradigm. The w1118 mutants learned slower than wildtype controls, yet with additional training, they reached wildtype levels of performance. The w1118 learning phenotype is also found in the wapricot and wcoral alleles, is dominant, and is rescued by genomic white and mini-white transgenes. Reducing dietary cholesterol strongly impaired olfactory learning for wildtype controls, while w1118 mutants were resistant to this deficit. The w1118 mutants displayed higher levels of cholesterol and cholesterol esters than wildtype under this low-cholesterol diet. Increasing levels of serotonin, dopamine, or both in the white mutants significantly improved w1118 learning. However, serotonin levels were not lower in the heads of the w1118 mutants than in wildtype controls. There were also no significant differences found in synapse numbers within the w1118 brain. We propose that the w1118 learning defect may be due to inefficient biogenic amine signaling brought about by altered cholesterol homeostasis.

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