Effect of diabetes on cholesterol and fatty acid synthesis in the rat aorta

1960 ◽  
Vol 198 (1) ◽  
pp. 25-28 ◽  
Author(s):  
Daniel W. Foster ◽  
Marvin D. Siperstein
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Cholesterol Synthesis ◽  
Acid Synthesis ◽  
Rat Aorta ◽  
Diabetic Rats ◽  
Liver Cholesterol ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis ◽  
Normal Controls

The synthesis of cholesterol and fatty acids from acetate-1-C14 was studied in the aortas and livers of 42 diabetic rats and their normal controls. Hepatic cholesterol synthesis was significantly increased in 13, decreased in 13, and unchanged in 16 of the 42 animals. Fatty acid synthesis was depressed in the liver in 39 of the 42 diabetic rats. Aortic cholesterogenesis was increased in only 2 of the 13 aortas from the same rats showing elevated hepatic cholesterol synthesis. Fatty acid synthesis was depressed in 21 of 42 aortas from the diabetic group. It is concluded, therefore, that the aorta is relatively resistant to stimulation of cholesterol synthesis by diabetes even when hepatic cholesterol synthesis in the same animal is elevated. Lipogenesis on the other hand is commonly depressed in the aorta as well as the liver. Cholesterol was purified through dibrominization and both normal and diabetic aortas were shown to be capable of carrying cholesterol synthesis to completion.

EFFECT OF ALLOXAN, INSULIN, AND THYROXINE ON CHOLESTEROL AND FATTY ACID SYNTHESIS BY RAT LIVER HOMOGENATES

1957 ◽  
Vol 35 (1) ◽  
pp. 15-23 ◽  
Author(s):  
J. F. Scaife ◽  
B. B. Migicovsky
Keyword(s):  
Carbon Dioxide ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthesis ◽  
Sodium Acetate ◽  
Cholesterol Synthesis ◽  
Acid Synthesis ◽  
Liver Homogenates ◽  
Vitro Effect

The in vitro effect of alloxan and insulin on the synthesis of cholesterol and fatty acids from 1-C14-sodium acetate by rat liver homogenates has been examined. Alloxan caused a reduction in the incorporation of acetate into cholesterol, fatty acids, and C14O2, but an increase in the oxygen consumption and carbon dioxide production. The addition of insulin to homogenates caused a reduction in cholesterol synthesis but an increase in fatty acid synthesis both for normal and diabetic animals. Homogenates from thyrotoxic rats exhibited a marked reduction in cholesterol synthesis when compared with normal animals. C14O2 production by homogenates from starved rats was appreciably lower than for those from normal animals. With this exception no appreciable difference was found in the oxygen uptake, carbon dioxide, or C14O2 production in homogenates from normal, starved, thyroxine-treated, or diabetic animals. Synthesized cholesterol was found to be located principally in the particulate matter of the homogenates after they had been incubated with 1-C14-sodium acetate. Homogenates from starved rats showed no greater tendency to degrade preformed cholesterol during incubation than did those from normal rats.

EFFECT OF ALLOXAN, INSULIN, AND THYROXINE ON CHOLESTEROL AND FATTY ACID SYNTHESIS BY RAT LIVER HOMOGENATES

1957 ◽  
Vol 35 (1) ◽  
pp. 15-23 ◽  
Author(s):  
J. F. Scaife ◽  
B. B. Migicovsky
Keyword(s):  
Carbon Dioxide ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Rat Liver ◽  
Fatty Acid Synthesis ◽  
Sodium Acetate ◽  
Cholesterol Synthesis ◽  
Acid Synthesis ◽  
Liver Homogenates ◽  
Vitro Effect

The in vitro effect of alloxan and insulin on the synthesis of cholesterol and fatty acids from 1-C14-sodium acetate by rat liver homogenates has been examined. Alloxan caused a reduction in the incorporation of acetate into cholesterol, fatty acids, and C14O2, but an increase in the oxygen consumption and carbon dioxide production. The addition of insulin to homogenates caused a reduction in cholesterol synthesis but an increase in fatty acid synthesis both for normal and diabetic animals. Homogenates from thyrotoxic rats exhibited a marked reduction in cholesterol synthesis when compared with normal animals. C14O2 production by homogenates from starved rats was appreciably lower than for those from normal animals. With this exception no appreciable difference was found in the oxygen uptake, carbon dioxide, or C14O2 production in homogenates from normal, starved, thyroxine-treated, or diabetic animals. Synthesized cholesterol was found to be located principally in the particulate matter of the homogenates after they had been incubated with 1-C14-sodium acetate. Homogenates from starved rats showed no greater tendency to degrade preformed cholesterol during incubation than did those from normal rats.

High plasma cholesterol in drug-induced cholestasis is associated with enhanced hepatic cholesterol synthesis

1999 ◽  
Vol 276 (5) ◽  
pp. G1165-G1173 ◽  
Author(s):  
Jeffrey W. Chisholm ◽  
Patrick Nation ◽  
Peter J. Dolphin ◽  
Luis B. Agellon
Keyword(s):  
Bile Acids ◽  
Cholesterol Synthesis ◽  
Cell Membranes ◽  
Reductase Activity ◽  
Plasma Cholesterol ◽  
Hepatic Cell ◽  
Plasma Lipoproteins ◽  
Liver Cholesterol ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis

In α-naphthylisothiocyanate-treated mice, plasma phospholipid (PL) levels were elevated 10- and 13-fold at 48 and 168 h, respectively, whereas free cholesterol (FC) levels increased between 48 h (17-fold) and 168 h (39-fold). Nearly all of these lipids were localized to lipoprotein X-like particles in the low-density lipoprotein density range. The PL fatty acyl composition was indicative of biliary origin. Liver cholesterol and PL content were near normal at all time points. Hepatic hydroxymethylglutaryl CoA reductase activity was increased sixfold at 48 h, and cholesterol 7α-hydroxylase activity was decreased by ∼70% between 24 and 72 h. These findings suggest a metabolic basis for the appearance of abnormal plasma lipoproteins during cholestasis. Initially, PL and bile acids appear in plasma where they serve to promote the efflux of cholesterol from hepatic cell membranes. Hepatic cholesterol synthesis is then likely stimulated in the response to the depletion of hepatic cell membranes of cholesterol. We speculate that the enhanced synthesis of cholesterol and impaired conversion to bile acids, particularly during the early phase of drug response, contribute to the accumulation of FC in the plasma.

scholarly journals THE EFFECT OF DIET ON HEPATIC CHOLESTEROL SYNTHESIS IN ALLOXAN DIABETIC RATS

1974 ◽  
Vol 20 (1) ◽  
pp. 71-79
Author(s):  
Yukihiro NAKABOU ◽  
Mayumi FUJIMOTO ◽  
Chiyo OKITA ◽  
Yasuo TAKANO ◽  
Hiroshi HAGIHIRA
Keyword(s):  
Cholesterol Synthesis ◽  
Diabetic Rats ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis

Effect of glucose or fructose feeding on cholesterol synthesis in diabetic animals

1985 ◽  
Vol 249 (5) ◽  
pp. G634-G641 ◽  
Author(s):  
K. R. Feingold ◽  
A. H. Moser
Keyword(s):  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
Active Form ◽  
Diabetic Rats ◽  
Hepatic Cholesterol ◽  
Hmg Coa Reductase ◽  
Hepatic Cholesterol Synthesis ◽  
Streptozotocin Induced Diabetes ◽  
Intestinal Hypertrophy ◽  
Coa Reductase

Previous studies have demonstrated that cholesterol synthesis is increased twofold in the small intestines of rats with streptozotocin-induced diabetes. The purpose of the present study was to determine the effect of adding glucose or fructose to standard rat chow on cholesterol synthesis in control and diabetic rats. In control rats a 25% glucose or fructose diet fed for 21 days markedly inhibited hepatic cholesterol synthesis in the liver. In contrast, in diabetic animals only fructose inhibited hepatic cholesterol synthesis. In both control and diabetic animals the addition of these simple sugars to the diet did not markedly alter extrahepatic cholesterol synthesis. The enhancement of small intestinal cholesterol synthesis observed in diabetic animals was present regardless of the dietary manipulations. Further studies demonstrated that the addition of smaller concentrations of fructose (10%) to standard rat chow decreased hepatic cholesterol synthesis in both control and diabetic rats. Similarly the addition of fructose to the diet of control and diabetics for a period as short as 2 days was also sufficient to inhibit hepatic cholesterol synthesis. In both control and diabetic animals, fructose feeding decreased hepatic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase activity but did not alter the percentage of HMG-CoA reductase in the active form. Finally, the intestinal hypertrophy and stimulation of intestinal cholesterogenesis that are characteristic of streptozotocin-induced diabetes occurred when either glucose or fructose was the sole caloric source.

scholarly journals Studies in lipogenesis in vivo. Fatty acid and cholesterol synthesis during starvation and re-feeding

1966 ◽  
Vol 101 (3) ◽  
pp. 811-818 ◽  
Author(s):  
GR Jansen ◽  
ME Zanetti ◽  
CF Hutchison
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Intraperitoneal Injection ◽  
Cholesterol Synthesis ◽  
Liver Glycogen ◽  
Acid Synthesis ◽  
Tracer Dose ◽  
Intraperitoneal Dose

1. Lipogenesis in vivo has been studied in mice given a 250mg. meal of [U-(14)C]glucose (2.5muc) or given an intraperitoneal injection of 25mug. of [U-(14)C]glucose (2.0muc). 2. The ability to convert a [U-(14)C]glucose meal into fatty acid was not significantly depressed by 6-7hr. of starvation. In contrast, incorporation of (14)C into fatty acid in the liver after the intraperitoneal dose of [(14)C]glucose was depressed by 80% and by more than 90% by 1 and 2hr. of starvation respectively. Carcass fatty acid synthesis from the [U-(14)C]glucose meal was not depressed by 12hr. of starvation, whereas from the tracer dose of [U-(14)C]glucose the depression in incorporation was 80% after 6hr. of starvation. 3. Re-feeding for 3 days, after 3 days' starvation, raised fatty acid synthesis and cholesterol synthesis in the liver fivefold and tenfold respectively above the levels in non-starved control mice. These increases were associated with an increased amount of both fatty acid and cholesterol in the liver. 4. After 18hr. of starvation incorporation of a [U-(14)C]glucose meal into carcass and liver glycogen were both increased threefold.

Extrahepatic lipogenesis contributes to hyperlipidemia in the analbuminemic rat

1993 ◽  
Vol 265 (1) ◽  
pp. F70-F76 ◽  
Author(s):  
J. A. Joles ◽  
K. R. Feingold ◽  
A. Van Tol ◽  
L. H. Cohen ◽  
X. Sun ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
Plasma Cholesterol ◽  
Liver Microsomes ◽  
Lipid Synthesis ◽  
Acid Synthesis ◽  
Apo Ai

Hepatic lipid and apolipoprotein synthesis is increased in the nephrotic syndrome. Catabolism of triglyceride-rich lipoproteins is impaired in nephrotic syndrome but not in rats with hereditary analbuminemia (NA), suggesting that lipid synthesis should be increased by analbuminemia in the absence of proteinuria. In this study the rate of cholesterol and fatty acid synthesis in liver and extrahepatic tissue was measured in female NA and control Sprague-Dawley (SD) rats to determine whether lipid synthesis was indeed increased in isolated analbuminemia and to identify the site(s) of increased lipogenesis. We also measured the concentrations of apolipoproteins (apo) AI, B, and E in plasma, as well as the levels of the respective mRNAs in liver. Plasma cholesterol, triglycerides, and apo AI, B, and E were all increased severalfold in the NA rat (P < 0.001). Although liver apolipoprotein mRNA content was significantly increased (P < 0.001) for apo AI (643%), B (273%), and E (299%), 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in liver microsomes and hepatic cholesterol synthesis were not significantly increased in the NA rats. Hepatic fatty acid synthesis and intestinal cholesterol synthesis were not increased in the NA rats. Surprisingly, intestinal fatty acid synthesis was elevated by 60% (P < 0.01). The NA rats demonstrated approximately fourfold increases in the incorporation of 3H2O into circulating cholesterol and fatty acids (P < 0.001). A 56% increase in the synthesis of total nonsaponifiable lipid was found in the extravisceral carcass (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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