Effects of a low-fat, high-carbohydrate diet on VLDL-triglyceride assembly, production, and clearance.
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Low-fat, high-carbohydrate (LF/HC) diets commonly elevate plasma triglyceride (TG) concentrations, but the kinetic mechanisms responsible for this effect remain uncertain. Subjects with low TG (normolipidemic [NL]) and those with moderately elevated TG (hypertriglyceridemic [HTG]) were studied on both a control and an LF/HC diet. We measured VLDL particle and TG transport rates, plasma nonesterified fatty acid (NEFA) flux, and sources of fatty acids used for the assembly of VLDL-TG. The LF/HC diet resulted in a 60% elevation in TG, a 37% reduction in VLDL-TG clearance, and an 18% reduction in whole-body fat oxidation, but no significant change in VLDL-apo B or VLDL-TG secretion rates. Significant elevations in fasting apo B-48 concentrations were observed on the LF/HC in HTG subjects. In both groups, fasting de novo lipogenesis was low regardless of diet. The NEFA pool contributed the great majority of fatty acids to VLDL-TG in NL subjects on both diets, whereas in HTG subjects, the contribution of NEFA was somewhat lower overall and was reduced further in individuals on the LF/HC diet. Between 13% and 29% of VLDL-TG fatty acids remained unaccounted for by the sum of de novo lipogenesis and plasma NEFA input in HTG subjects. We conclude that (a) whole-food LF/HC diets reduce VLDL-TG clearance and do not increase VLDL-TG secretion or de novo lipogenesis; (b) sources of fatty acids for assembly of VLDL-TG differ between HTG and NL subjects and are further affected by diet composition; (c) the presence of chylomicron remnants in the fasting state on LF/HC diets may contribute to elevated TG levels by competing for VLDL-TG lipolysis and by providing a source of fatty acids for hepatic VLDL-TG synthesis; and (d) the assembly, production, and clearance of elevated plasma VLDL-TG in response to LF/HC diets therefore differ from those for elevated TG on higher-fat diets. (+info)
Heterogeneity in associations between macronutrient intake and lipoprotein profile in individuals with type 2 diabetes.
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OBJECTIVE: To evaluate associations between macronutrient intake and lipoprotein profile among individuals with type 2 diabetes who participated in the San Luis Valley Diabetes Study (SLVDS) or the Insulin Resistance Atherosclerosis Study (IRAS). RESEARCH DESIGN AND METHODS: Diet was assessed by 24-h recall in the SLVDS (n = 421) and by validated food frequency interview in the IRAS (n = 437). Analyses adjusted for kilocalories, age, sex, and other covariates were conducted separately for the two study groups. For the SLVDS, repeated observations were included in mixed model analyses (865 observations). For the IRAS, standard regression analyses were conducted. Recent weight history and time of diabetes diagnosis were evaluated as possible modifiers of associations between nutrient intake and lipoprotein profile. RESULTS: Higher reported intake of total dietary fat was related to significantly higher levels of LDL cholesterol (P < 0.05) in both studies and in all subgroups. Reported intake of total and saturated fat was associated positively with total cholesterol, although statistical significance was not reached for all subgroups. Higher reported carbohydrate intake was associated with increased triglyceride concentrations (P < 0.01) only among individuals with previously undiagnosed diabetes in the SLVDS (n = 69) and only among individuals who gained weight (> 5 lb, n = 87) during the previous year in the IRAS. CONCLUSIONS: Toward the goal of optimizing the lipoprotein profile of individuals with diabetes, these results emphasize the potential importance of reducing fat intake while recognizing that individualized approaches to diet are important to minimize the risk of cardiovascular disease. (+info)
Role of lipid type on morphine-stimulated diet selection in rats.
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Administration of morphine is said to increase fat consumption among rats allowed to self-select nutrients. However, fats represent a diverse group of molecules, differing in metabolic and sensory properties. Despite this, lipid has yet to be manipulated as a variable in drug-stimulated nutrient selection studies. To determine whether lipid source can impact daily and morphine-stimulated (1, 3, and 10 mg/kg) diet intake, rats were provided with a choice between a high-fat and high-carbohydrate diet in three regimens in which the source of fat was varied between vegetable shortening, lard, or corn oil. Daily and morphine-stimulated diet selections were determined under all conditions. Under daily feeding conditions, rats ate more of the high-lipid diet compared with the high-carbohydrate diet when vegetable shortening or lard was the main lipid alternative, but lipid and carbohydrate intake did not differ when corn oil was the main lipid alternative. When rats were stimulated with morphine, the percentage of lipid increased relative to baseline intake only when the lipid diets were the preferred alternatives (i.e., vegetable shortening or lard). When preference between lipid and carbohydrate diets was neutral (i.e., corn oil condition), morphine did not enhance lipid consumption. These results indicate that morphine increases consumption of total energy or preferred diets and not lipid per se. (+info)
Blood sugar formation from dietary carbohydrate is facilitated by the pentose phosphate pathway in an insect Manduca sexta Linnaeus.
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Dietary carbohydrate, the principal energy source for insects, also determines the level of the blood sugar trehalose. This disaccharide, a byproduct of glycolysis, occurs at highly variable concentrations that play a key role in regulating feeding behavior and growth. Little is known of how developing insects partition the metabolism of dietary carbohydrate to meet the needs for blood trehalose, ribose sugars and NADPH, as well as energy production. This study examined the effects of varying dietary sucrose levels between 3.4 and 34 g/l in an artificial diet on growth rate, depot fat content and blood sugar formation from (13)C-enriched glucose in Manduca sexta. (2-(13)C)Glucose or (1,2-(13)C(2))glucose were administered to larvae by injection and after 6 h blood was analyzed by nuclear magnetic resonance spectroscopy. [2-(13)C]Trehalose was the principal product of [2-(13)C]glucose, but trehalose was also (13)C-enriched at C1 and C3, demonstrating activity of the pentose phosphate pathway. The trehalose C1/C2 (13)C-enrichment ratio, a measure of the substrate cycled through the pentose pathway, significantly increased with increasing dietary sugar, and reached a mean of 0.22 at the highest level. Blood trehalose concentration increased from approximately 38 mM at the lowest dietary carbohydrate level to 75 mM at the highest. Moreover, blood trehalose, growth rate and depot fat all increased in precisely the same way in relation to the level of pentose cycling. Based on the multiplet (13)C-NMR signal structure of trehalose synthesized from [1,2-(13)C(2)]glucose by insects maintained on a high carbohydrate diet, it was established that the formation of trehalose from glucose phosphate derived directly from the administered substrate, with no involvement of the pentose pathway, was greater than that from glucose phosphate metabolized through the pentose pathway prior to trehalose synthesis. On the other hand, glucose phosphate first metabolized through the pentose pathway contributed more to pyruvate formation than did glucose phosphate formed from the labeled substrate metabolized directly to pyruvate via glycolysis; this finding based on the multiplet (13)C-NMR signal structure in alanine derived from pyruvate. The results suggest that as dietary carbohydrate increases blood sugar synthesis from glucose phosphate derived directly from dietary sugar is facilitated by the pentose pathway which provides an increasing amount of substrate to pyruvate formation. (+info)
Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake.
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To assess the impact of the macronutrient content of a meal on the postprandial leptin response and its relationship with postprandial satiety, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. Blood sampling and hunger and satiety scores were collected hourly during 9 h after the meal. Spontaneous intake was measured at a buffet meal at 9 h postprandially. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In women, leptin levels were higher after the fat meal than while fasting. Leptin response was significantly correlated to insulin response (r = 0.51, P < 0.0001). Hunger and satiety ratings and subsequent energy intake were not different after carbohydrate or fat intake. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal. Short-term regulation of postprandial satiety and food intake is not influenced by circulating leptin. (+info)
Rate and extent of digestion of the ethanol-soluble and neutral detergent-insoluble fractions of corn grain.
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The objectives of this study were to partition corn grain into three digestible fractions and to measure the rate of disappearance of these fractions in vitro. Seventeen corn grain samples with varied fiber concentrations were extracted with either 80% ethanol or neutral detergent to obtain estimates of the pool size and digestion kinetics of the A, B1, B2, and C fractions. The carbohydrate soluble in 80% ethanol averaged only 2.6+/-.3% of the DM, although 80% ethanol extracted 7.1+/-1.2% of DM of corn grain. The ethanol-soluble fraction of corn grain contained protein, ether-extractable compounds, and a small amount of ash in addition to carbohydrate. Because of this chemical heterogeneity and because of the small size of the ethanol-soluble fraction, it was not possible to determine the digestion rate of this fraction by measuring gas production. The NDF content of the corn grain was 10.6+/-.7% of DM and was highly digestible (94.6+/-1.4%). The digestible NDF contributed 9.5% of the total gas production from corn grain. Because the size, digestibility, and digestion rate of the digestible NDF fraction varied little among corn grain samples, it is not necessary to routinely analyze the digestion kinetics of the digestible NDF fraction of dried corn grain. An average gas production curve of this fraction can be used as a base to subtract from the total gas production curve to generate the gas production curve of the neutral detergent-soluble fraction for dried, ground corn grain samples. (+info)
Refined-cereal intake and risk of selected cancers in italy.
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BACKGROUND: Although consumption of whole-grain foods seems to reduce the risk of several types of neoplasms, the potential influence of a diet rich in starches and refined grains is less clear. OBJECTIVE: We studied the relation between the frequency of consumption of refined cereals (bread, pasta, or rice) and the risk of selected neoplasms. DESIGN: This was an integrated series of case-control studies conducted in northern Italy between 1983 and 1993. The subjects were patients admitted to the major teaching and general hospitals in Milan and Pordenone with incident, histologically confirmed cancers: 343 with cancer of the oral cavity and pharynx, 94 with cancer of the esophagus, 146 with cancer of the larynx, 745 with cancer of the stomach, 955 with cancer of the colon, 625 with cancer of the rectum, and 428 with cancer of the thyroid. The control subjects were 3526 patients admitted to the same network of hospitals for acute nonneoplastic conditions unrelated to long-term modification of diet. Odds ratios (ORs) for consecutive tertiles of refined-cereal consumption were computed after allowance for sociodemographic variables, education, smoking status, alcohol consumption, body mass index, and consumption of fruit, vegetables, and whole-grain foods. RESULTS: The ORs for the highest tertile of refined-cereal intake were 1.6 for cancer of the oral cavity, pharynx, esophagus, or larynx; 1.5 for stomach cancer; 1.5 for colon cancer; 1.3 for cancer of the rectum; and 2.0 for thyroid cancer. The trends in risk were significant for all neoplasms considered. CONCLUSION: Consumption of refined cereals was associated with an increased risk of cancers of the large bowel, the stomach, and other selected digestive and nondigestive sites. (+info)
A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids.
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Dietary polyunsaturated fatty acids (PUFA) are negative regulators of hepatic lipogenesis that exert their effects primarily at the level of transcription. Sterol regulatory element-binding proteins (SREBPs) are transcription factors responsible for the regulation of cholesterol, fatty acid, and triglyceride synthesis. In particular, SREBP-1 is known to play a crucial role in the regulation of lipogenic gene expression in the liver. To explore the possible involvement of SREBP-1 in the suppression of hepatic lipogenesis by PUFA, we challenged wild-type mice and transgenic mice overexpressing a mature form of SREBP-1 in the liver with dietary PUFA. In the liver of wild-type mice, dietary PUFA drastically decreased the mature, cleaved form of SREBP-1 protein in the nucleus, whereas the precursor, uncleaved form in the membranes was not suppressed. The decreases in mature SREBP-1 paralleled those in mRNAs for lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase. In the transgenic mice, dietary PUFA did not reduce the amount of transgenic SREBP-1 protein, excluding the possibility that PUFA accelerated the degradation of mature SREBP-1. The resulting sustained expression of mature SREBP-1 almost completely canceled the suppression of lipogenic gene expression by PUFA in the SREBP-1 transgenic mice. These results demonstrate that the suppressive effect of PUFA on lipogenic enzyme genes in the liver is caused by a decrease in the mature form of SREBP-1 protein, which is presumably due to the reduced cleavage of SREBP-1 precursor protein. (+info)