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hypertriglyceridemia/carbohydrate
Link salvestatakse lõikelauale
Leht 1 alates 476 tulemused
Reversal of severe hypertriglyceridemia with intermittent fasting and a very-low-carbohydrate ketogenic diet: a case series
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Logi sisse
Purpose of review: To illustrate successful reversal of hypertriglyceridemia using a very-low-carbohydrate ketogenic diet in conjunction with intermittent fasting in two patients.
Recent findings:
Effect of somatostatin-induced suppression of postprandial insulin response upon the hypertriglyceridemia associated with a high carbohydrate diet.
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In an attempt to define the relationship between plasma insulin and triglyceride concentrations, we have studied the effect of suppression of the postprandial insulin response upon the secretion and plasma concentration of very low density lipoprotein (VLDL)-triglycerides. Eight nondiabetic subjects
Treatment of hypertriglyceridemia by two diets rich either in unsaturated fatty acids or in carbohydrates: effects on lipoprotein subclasses, lipolytic enzymes, lipid transfer proteins, insulin and leptin.
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BACKGROUND
There is lack of agreement on which dietary regimen is most suitable for treatment of hypertriglyceridemia, especially if high triglyceride concentrations are not due to obesity or alcohol abuse. We compared the effects on blood lipids of a diet high in total and unsaturated fat with a
Long-term effect of a low-fat, high-carbohydrate diet on plasma lipids of patients affected by familial endogenous hypertriglyceridemia.
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Logi sisse
We evaluated the effect of a low-fat, high carbohydrate (LFHC) diet on plasma lipids in 10 patients affected by familial endogenous hypertriglyceridemia. All the patients studied underwent a base-line period of 4 wk, a 12-wk intervention period, and an 8-wk switch-back period. During the control
Carbohydrate-induced hypertriglyceridemia: an insight into the link between plasma insulin and triglyceride concentrations.
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This study was initiated to test the hypothesis that endogenous hypertriglyceridemia results from a defect in the ability of insulin to inhibit the release of very low-density lipoprotein-triglyceride (TG) from the liver. To accomplish this goal, plasma glucose, insulin, free fatty acid (FFA), and
A crossover trial of high and low sucrose-carbohydrate diets in type II diabetics with hypertriglyceridemia.
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Logi sisse
Earlier work shows that hyperlipemic type II diabetics tolerate wide ranges of sucrose and carbohydrate intake without effects on glycemic control, but a rise of fasting serum triglycerides sometimes occurs. To address further the issue of individual susceptibility to carbohydrate, the current study
Will a high-carbohydrate, low-fat diet lower plasma lipids and lipoproteins without producing hypertriglyceridemia?
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A sudden increase in dietary carbohydrate invariably increases the plasma levels of very low density lipoprotein (VLDL) and triglyceride. The present studies were designed to test the hypothesis that dietary carbohydrate-induced hypertriglyceridemia need not occur. In the first study we fed
Dietary fiber prevents carbohydrate-induced hypertriglyceridemia.
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Logi sisse
Plant foods rich in carbohydrate and dietary fiber have many health benefits. One concern often expressed about higher carbohydrate, lower fat diets is that they may increase fasting serum triglycerides. Recently the importance of hypertriglyceridemia as an independent risk factor for coronary heart
Mechanism of carbohydrate-induced hypertriglyceridemia: plasma lipid metabolism in mice.
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A group of mice were fed on a basal diet for 2 wk and thereafter maintained on a fat free high sucrose or starch diet for 5-6 wk. Hypertriglyceridemia was induced in the mice on feeding the high carbohydrate diets. The triglyceride levels reached maximum in 12 and 14-18 days on high sucrose and
Inhibition of carbohydrate-induced hypertriglyceridemia by metformin.
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The ability of metformin to prevent carbohydrate-induced hypertriglyceridemia was studied in fructose fed rats. The results indicated that plasma triglycerides were approximately 50% reduced in the drug treated rats and the reduction was associated with lowered very low density
[Regression of xanthomas in endogenous hypertriglyceridemia under low carbohydrate diet].
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Report on two patients with endogenous hypertriglyceridemia. In both patients normal serum lipid values were reached in a comparatively short time under a diet with reduced carbohydrates and calories. In one diabetic patient who needed insulin at the beginning of the treatment the disease could be
Reduction of carbohydrate-induced hypertriglyceridemia in (fa,fa) "Zucker" rats by the alpha-glucosidase inhibitor acarbose (BAY g 5421).
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Logi sisse
Inhibition of carbohydrate digestion by the alpha-glucosidase inhibitor acarbose (BAY g 5421)reduces carbohydrate-induced postprandial blood glucose increase and insulin secretion. As a consequence, in feeding experiments sucrose-induced hyperinsulinemia and hypertriglyceridemia in genetically obese
Hypertriglyceridemia and carbohydrate intolerance: interrelations and therapeutic implications.
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Logi sisse
Atherosclerosis, the most frequent complication of diabetes, could be the result of hyperlipidemia, among other factors. Mounting evidence suggests that reducing the concentration of triglyceride-rich lipoprotein, which influences the production of the possibly atherogenic intermediate density
Ability of exercise to inhibit carbohydrate-induced hypertriglyceridemia in rats.
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The ability of spontaneous running to prevent carbohydrate-induced hypertriglyceridemia was studied in young, nonobese rats. Exercise-trained and sedentary rats were fed a diet consisting of (as percent total calories) 12% fat, 22% protein, and 66% carbohydrate. The source of the carbohydrate was
Dose-response effects of dietary marine oil on carbohydrate and lipid metabolism in normal subjects and patients with hypertriglyceridemia.
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Logi sisse
Recent studies indicate that marine (omega-3) fatty acids decrease hypertriglyceridemia but worsen hyperglycemia in diabetes. We studied dose-response relationships between omega-3 intake and indices of carbohydrate and lipid metabolism in 21 hypertriglyceridemic patients with (n = 6) or without (n
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