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Hypertriglyceridemia:
5 Abstracts
Am J Clin Nutr 2003 Jan;77(1):43-50
Hepatic de novo lipogenesis in normoinsulinemic
and hyperinsulinemic subjects consuming high-fat, low-carbohydrate
and low-fat, high- carbohydrate isoenergetic diets. |
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Schwarz
JM, Linfoot P, Dare D, Aghajanian K.
Department of Nutritional Sciences and Toxicology, University of California,
Berkeley (J-MS and KA), and the Department of Medicine, University of California,
San Francisco (J-MS, PL, and DD). |
| BACKGROUND:
Hypertriglyceridemia is associated with increased risk of cardiovascular
disease. Until recently, the importance of hepatic de novo lipogenesis
(DNL) in contributing to hypertriglyceridemia was difficult to
assess because of methodologic limitations. OBJECTIVE: We evaluated
the extent of the contribution by DNL to different conditions associated
with hypertriglyceridemia. DESIGN: After 5 d of an isoenergetic
high-fat, low-carbohydrate diet, fasting DNL was measured in normoinsulinemic
(</= 85 pmol/L) lean (n = 9) and obese (n = 6) and hyperinsulinemic
(>/= 115 pmol/L) obese (n = 8) subjects. Fasting DNL was measured
after a low-fat, high- carbohydrate diet in normoinsulinemic lean
(n = 5) and hyperinsulinemic obese (n = 5) subjects. Mass isotopomer
distribution analysis was used to measure the fraction of newly
synthesized fatty acids in VLDL-triacylglycerol. RESULTS: With
the high-fat, low- carbohydrate diet, hyperinsulinemic obese subjects
had a 3.7-5.3-fold higher fractional DNL (8.5 +/- 0.7%) than did
normoinsulinemic lean (1.6 +/- 0.5%) or obese (2.3 +/- 0.3%) subjects.
With the low-fat, high-carbohydrate diet, normoinsulinemic lean
and hyperinsulinemic obese subjects had similarly high fractional
DNL (13 +/- 5.1% and 12.8 +/- 1.4%, respectively). Compared with
baseline, consumption of the high-fat, low- carbohydrate diet did
not affect triacylglycerol concentrations. However, after the low-fat,
high-carbohydrate diet, triacylglycerols increased significantly
and DNL was 5-6-fold higher than in normoinsulinemic subjects consuming
a high-fat diet. The increase in triacylglycerol after the low-fat,
high-carbohydrate diet was correlated with fractional DNL (P < 0.01),
indicating that subjects with high DNL had the greatest increase
in triacylglycerols. CONCLUSIONS: These results support the concept
that both hyperinsulinemia and a low-fat diet increase DNL, and
that DNL contributes to hypertriglyceridemia. |
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| PMID:
12499321 [PubMed - in process] |
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Arterioscler
Thromb Vasc Biol 2001 Sep;21(9):1520-5
Exercise prevents the accumulation of triglyceride-rich lipoproteins
and their remnants seen when changing to a high-carbohydrate diet.
Koutsari C, Karpe F, Humphreys SM, Frayn KN, Hardman AE.
Human Muscle Metabolism Research Group, Loughborough University, Loughborough,
UK.
We tested the hypothesis that daily aerobic exercise opposes the fasting hypertriglyceridemia
and exaggerated postprandial lipemia observed after substituting dietary fat
with carbohydrate. Eight healthy postmenopausal women aged 51 to 66 years consumed
the same high-fat mixed meal on 3 occasions: (1) after 3 days on a low- carbohydrate
diet (35%, 50%, and 15% energy from carbohydrate, fat, and protein, respectively);
(2) after 3 days on an isoenergetic high-carbohydrate diet (corresponding values
70%, 15%, and 15%); and (3) after 3 days on the same high-carbohydrate diet with
60 minutes of brisk walking daily. Plasma triglycerides were higher after the
high- carbohydrate diet than after the low-carbohydrate diet: fasting, 1.58+/-0.19
versus 0.96+/- 0.12 mmol/L, respectively; 6-hour postprandial area under concentration
versus time curve, 13.74+/-1.57 versus 10.12+/-1.15 (mmol/L)xhour, respectively
(both P<0.01). In the fasted and postprandial states, concentrations of apolipoproteins
B-48 and B-100 in the triglyceride-rich lipoprotein fraction were significantly
higher after the high- carbohydrate diet, as was the concentration of remnant-like
lipoprotein particle cholesterol (a measure of lipoprotein remnants). These carbohydrate-induced
increases in the number of circulating triglyceride-rich particles and their
remnants were abolished when subjects had exercised daily during the high-carbohydrate
diet.
PMID: 11557682 [PubMed - indexed for MEDLINE] |
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J
Am Coll Nutr 2000 Jun;19(3):383-91
Fasting lipoprotein and postprandial triacylglycerol responses
to a low- carbohydrate diet supplemented with omega-3 fatty acids.
Volek JS, Gomez AL, Kraemer WJ.
The Human Performance Laboratory, Ball State University, Muncie, Indiana 47306,
USA.
BACKGROUND: The effects of a prolonged low-carbohydrate diet rich in omega-3 fatty
acids on blood lipid profiles have not been addressed in the scientific literature.
OBJECTIVE: This study examined the effects of an eight-week ketogenic diet rich
in omega-3 fatty acids on fasting serum lipoproteins and postprandial triacylglycerol
(TG) responses. DESIGN: Ten men consumed a low-carbohydrate diet rich in monounsaturated
fat (MUFA) and supplemented with omega-3 fatty acids for eight weeks. Fasting blood
samples were collected before and after one week of habitual diet and on two
consecutive days after 2, 4, 6 and 8 weeks of the intervention diet. Postprandial
TG responses to a fat-rich test meal were measured prior to and after the intervention
diet. RESULTS: Compared to the habitual diet, subjects consumed significantly
(p < or = 0.05) greater quantities of protein, fat, MUFA and omega-3 fatty acids
and significantly less total energy, carbohydrate and dietary fiber. Body weight
significantly declined over the experimental period (-4.2+/-2.7 kg). Compared
to baseline, fasting total cholesterol, LDL cholesterol and HDL cholesterol were
not significantly different after the intervention diet (+1.5%, +9.7% and +10.0%,
respectively). Fasting TG were significantly reduced after the intervention diet
(-55%). There was a significant reduction in peak postprandial TG (-42%) and
TG area under the curve (-48%) after the intervention diet. CONCLUSIONS: A hypocaloric
low- carbohydrate diet rich in MUFA and supplemented with omega-3 fatty acids significantly
reduced postabsorptive and postprandial TG in men that were not hypertriglyceridemic
as a group before the diet. This may be viewed as a clinically significant positive
adaptation in terms of cardiovascular risk status. However, transient increases
in total cholesterol and LDL cholesterol were also evident and should be examined
further in regard to which particular subfractions are elevated.
PMID: 10872901 [PubMed - indexed for MEDLINE] |
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Am J Physiol 1987 Dec;253(6 Pt 1):E664-9
Effect of carbohydrate intake on de novo lipogenesis in human
adipose tissue.
Chascione C, Elwyn DH, Davila M, Gil KM, Askanazi J, Kinney JM.
Department of Surgery, College of Physicians and Surgeons, Columbia University,
New York, New York 10032.
Rates of synthesis, from [14C]glucose, of fatty acids (de novo lipogenesis) and
glycerol (triglyceride synthesis) were measured in biopsies of adipose tissue
from nutritionally depleted patients given low- or high-carbohydrate intravenous
nutrition. Simultaneously, energy expenditure and whole-body lipogenesis were
measured by indirect calorimetry. Rates of whole-body lipogenesis were zero on
the low-carbohydrate diet and averaged 1.6 g.kg-1.day-1 on the high-carbohydrate
diet. In vitro rates of triglyceride synthesis increased 3-fold going from the
low to the high intake; rates of fatty acid synthesis increased approximately
80-fold. In vitro, lipogenesis accounted for less than 0.1% of triglyceride synthesis
on the low intake and 4% on the high intake. On the high- carbohydrate intake,
in vitro rates of triglyceride synthesis accounted for 61% of the rates of unidirectional
triglyceride synthesis measured by indirect calorimetry. In vitro rates of lipogenesis
accounted for 7% of whole-body lipogenesis. Discrepancies between in vitro rates
of fatty acid synthesis from glucose, compared with acetate and citrate, as reported
by others, suggest that in depleted patients on hypercaloric high-carbohydrate
diets, adipose tissue may account for up to 40% of whole-body lipogenesis.
PMID: 3122584 [PubMed - indexed for MEDLINE] |
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Versicherungsmedizin
1995 Aug 1;47(4):116-22
Comment in:
Versicherungsmedizin. 1995 Dec 1;47(6):231-3.
[Nutrition and coronary heart disease: how important is diet?]
[Article in German]
Worm N.
Three saturated fatty acids (C 12:0, C 14:0, C 16:0) raise LDL cholesterol but
also HDL cholesterol levels. Replacement of these fatty acids by monounsaturated
or omega-6 polyunsaturated fatty acids will lower LDL cholesterol as well as
HDL cholesterol levels. Fat modified diets therefore may not improve the ratio
of LDL to HDL cholesterol. Linoleic acid enhances sterol excretion but also increases
cholesterol synthesis so that total body cholesterol is not diminished. Moreover
various potentially adverse effects have been reported for omega-6 polyunsaturated
fatty acids. Recent cross-cultural ecologic studies as well as all major within-population
cohort studies have not been able to find an association between cholesterol
raising saturated fatty acids of animal fat and risk of Coronary Heart Disease
(CDH). On the other hand several cohort and case control studies have shown an
increase in CHD risk with increasing consumption of partly hydrogenated vegetable
margarines. Meta-analyses of controlled intervention studies reveal that cholesterol
lowering diets have failed to lower risk of CHD or total mortality. Yet controlled
studies implementing a high level of antioxidants in the diet or increasing the
omega-3 unsaturated fatty acid content have been able to lower CHD and total mortality.
It is time to discuss whether the concept of dietary intervention with the "classic" cholesterol
lowering diet is still justified.
Publication Types:
Review
Review, Tutorial
PMID: 7676547 [PubMed - indexed for MEDLINE] |
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