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1.
Effects of dietary triolein and sunflower oil on insulin release and lipid metabolism in zucker rats
Obese and lean male Zucker rats were fed ad libitum on diets containing either 50 (L) or 200 (H) g/kg diet of either triolein
(T) or sunflowerseed oil (S). The specific activity of the hepatic microsomal Δ9 desaturase enzyme was depressed in both lean
and obese rats fed the HS diet compared with the other three diets. The fatty acid composition of liver and subcutaneous white
adipose tissue lipids were consistent with a lower Δ9 desaturation activity in rats fed the H diets, particularly for the
HS diet. In both genotypes, microsomal Δ9 desaturase activity and the ratio of 16∶1/(16∶0+16∶1) fatty acids in liver lipids
were inversely related to the proportion of 18∶2 in liver lipid. Plasma insulin concentrations and rates of glucose-stimulated
insulin release in vivo were higher in obese rats compared with lean rats, and plasma insulin levels were higher in rats fed
S compared with T. There was no relationship between Δ9 desaturase activity and either plasma insulin concentration or rates
of insulin release in vitro. These findings suggest that hepatic Δ9 desaturase activity of Zucker rats is responsive to changes
in the proportion of 18∶2 in liver lipids but is not affected by changes in insulin secretion. 相似文献
2.
Aspects of the lipid metabolism of male, obese and lean Zucker rats were compared using animals which had been fed ad libitum
for 32 days on a diet (HS) which contained 200 g sunflowerseed oil/kg or one (LS) which contained 50 g/kg of the oil. When
compared with the LS diet, the HS diet decreased the characteristic lipid accretion in the liver of obese rats from 126 mg
(LS) to 81 mg (HS)/g wet weight; corresponding values for the lean rats were 39 mg and 56 mg/g wet weight of liver, respectively.
The HS diet depressed lipid synthesis de novo by liver homogenates and decreased the Δ9-desaturase activity of liver microsomes
from obese and clean rats by about 50%. Δ9-Desaturase activity in vitro was also depressed by the addition of linoleic acid
to liver microsomes from both obese and lean rats fed ad libitum on a standard laboratory diet. Depressed Δ9-desaturase activity,
due to ingestion of the HS diet, was reflected in lower ratios of 16∶1/16∶0 and 18∶1/18∶0 fatty acids in tissue lipids from
obese and lean rats. Ingestion of the HS compared with the LS diet resulted in increased proportions of 18∶2ω6 in liver lipids
and adipose tissue triacylglycerols of obese and lean rats. The HS diet also increased the proportions of 20∶4ω6 in adipose
triacylglycerols of obese and lean rats and in liver lipids of obese animals but not in their lean littermates. 相似文献
3.
Dietary CLA has been shown to enhance glucose tolerance in several animal models, but in mice it induces insulin resistance
and lipodystrophy. In this study, the effects of 2 wk of diet supplementation with either 1,5% CLA or 0.2% troglitazone (TZD),
an insulin-sensitizing thiazolidinedione, on glucose tolerance, lipid accumulation, and composition of both lean and Zucker
diabetic fatty (fa/fa; ZDF) rats were examined. Compared with lean rats, which maintained normal glucose tolerances after 2 wk of feeding regardless
of diet, ZDF rats fed a control diet (CON) had significantly worsened glucose tolerance. ZDF rats fed CLA and TZD diets, however,
maintained normal glucose tolerances. In contrast to the significantly elevated lipid levels in ZDF rats fed the CON diet,
concentrations of plasma FFA and TG in ZDF rats fed CLA and TZD diets were normalized. A similar reduction of plasma lipid
levels was observed in lean rats fed CLA and TZD compared with lean rats fed the CON diet. Although ZDF CON rats developed
significant hepatic steatosis, both CLA-and TZD-fed rats had hepatic TG levels similar to those of lean rats. Both lean and
ZDF rats fed the CLA diet had reduced adipose mass compared with respective genotype controls; however, TZD had no effect.
Ratios of 16∶1/16∶0 and 18∶1/18∶0 FA, surrogate markers for stearoyl-CoA desaturase-1 (SCD-1) activity, were reduced in livers
of ZDF rats fed CLA and TZD diets. These results show that, like TZD, CLA normalizes glucose tolerance and plasma lipids and
also improves hepatic steatosis and FA composition in ZDF rats. The effects of CLA and TZD on hepatic lipid composition suggest
that the effects of these two agents on glucose tolerance may be associated with a reduction in SCD-1. 相似文献
4.
Changes in a number of morphological and biochemical parameters were observed in genetically obese Zucker rats and in lean
controls between 3 and 58 weeks of age. By 3 weeks, the genetically obese rats had higher proportional (wt/100 g body wt)
and absolute amounts of adipose tissue, hyperlipemia affecting all the lipid fractions, and hyperproteinemia compared to lean
controls. Obesity, hepatomegaly, high concentrations of hepatic lipids and hyperinsulinemia did not appear until the fifth
week. In obese animals, liver lipid concentration reached a maximum at 17 weeks of age and then declined. During this time,
the triacylglycerol concentrations in the serum remained stable, whereas the cholesterol and phospholipid concentrations continued
to increase. The glycogen concentration in obese animals increased, both absolutely and compared to lean controls, between
the 12th and 43rd week of age. From weaning, the Zucker rats, compared to lean controls, exhibited characteristics of obesity
(accumulation of adipose tissue, hyperlipemia and hyperproteinemia), which persisted to the age of 58 weeks. 相似文献
5.
CLA has been shown to induce or suppress excess liver lipid accumulation in various animal models. Interestingly, the state
of insulin resistance may be an important modulator of this effect. The objective of the current study was to determine how
feeding a dietary CLA mixture would affect liver lipid accumulation in insulin-resistant/obese and lean rats in relation to
liver function, lipidemia, liver TAG and phospholipid FA composition, and expression of hepatic markers of FA transport, oxidation,
and synthesis. Six-week-old fa/fa and lean Zucker rats (n=20/genotype) were fed either a 1.5% CLA mixture or a control diet for 8 wk. CLA supplementation reduced liver lipid concentration
of fa/fa rats by 62% in concurrence with improved liver function (lower serum alanine aminotransferase and alkaline phosphatase) and
favorable modification of the serum lipoprotein profile (reduced VLDL and LDL and elevated HDL) compared with control-fed
fa/fa rats. The fa/fa genotype had two-thirds the amount of CLA (as % total FA) incorporated into liver TAG and phospholipids compared with the
lean genotype. In both genotypes, CLA altered the hepatic FA profile (TAG greater than phospholipids) and these changes were
explained by a desaturase enzyme index. Liver-FA-binding protein and acyl CoA oxidase, markers of FA transport and oxidation,
respectively, were expressed at higher levels in CLA-fed fa/fa rats. In summary, these results illustrate a strong relationship between the state of insulin resistance and liver lipid
metabolism and suggest that CLA acts to favorably modify lipid metabolism in fa/fa Zucker rats. 相似文献
6.
The regulation of palmitoyl-CoA chain elongation (PCE) by clofibric acid [2-(4-chlorophenoxy)-2-methylpropionic acid] was
investigated in comparison with stearoyl-CoA desaturase (SCD) in the liver of obese Zucker fa/fa rats. The proportion of oleic
acid in the hepatic lipids of Zucker obese rats is 2.7 times higher than that of lean littermates. The activities of PCE and
SCD in the liver of Zucker obese rats were markedly higher than in lean rats, and the hepatic uptake of 2-deoxyglucose (2-DG)
was also higher in Zucker obese rats compared with lean rats. The increased activities of SCD and PCE in Zucker obese rats
were due to the enhanced expression of mRNA of rELO1. The proportion of oleic acid in the liver was significantly increased
by the administration of clofibric acid to Zucker obese rats, and the hepatic PCE activity and rELO2 mRNA expression, but
not the SCD activity or SCD1 mRNA expression, were increased in response to clofibric acid treatment. By contrast, the activities
of both PCE and SCD and the mRNA expression of SCD1 and rELO2 in the liver were increased by the treatment of Zucker lean
rats with clofibric acid. Multiple regression analysis, which was performed to determine the relationships involving PCE activity,
SCD activity, and the proportion of oleic acid, revealed that the three parameters were significantly correlated and that
the standardized partial regression coefficient of PCE was higher than that of SCD. These results indicate that oleic acid
is synthesized by the concerted action of PCE and SCD and that PCE plays a crucial role in the formation of oleic acid when
Zucker fa/fa rats are given clofibric acid. 相似文献
7.
Subhash C. Jamdar 《Lipids》1979,14(5):463-468
Age-related changes in hepatic and adipose glycerolipid formation have been described in Zucker rats. Glycerolipid formation
was measured in vitro in the presence of [14C]glycerol-3-phosphate, palmitate, ATP, CoA, and Mg2+ by using liver and adipose tissue homogenates derived from various age groups of animals. Hepatic glycerolipid formation
increased after birth to reach a peak value at 1 day of age. This period was followed by a decline in the rates of glycerolipid
formation. Hepatic glycerolipid formation increased again at the time of weaning and continued to rise up to 32 days in lean
rats and 42–44 days in obese rats. Obesity in rats was recognizable at the age of 32 days and was associated with increased
rates of glycerolipid formation in both liver and adipose tissue. As far as the changes in hepatic glycerolipid formation
and triglyceride accumulation are concerned, obese rats showed more resemblance to 1-day-old rats than to lean animals of
similar age groups. Glycerolipid formation decreased in liver and increased in adipose tissue with age in both lean and obese
rats. These studies suggest that hepatic and adipose tissue glycerolipid formation is significantly influenced by age and
obesity in Zucker rats. 相似文献
8.
Nirajan Shrestha Josif Vidimce Olivia J. Holland James S. M. Cuffe Belinda R. Beck Anthony V. Perkins Andrew J. McAinch Deanne H. Hryciw 《International journal of molecular sciences》2021,22(6)
Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. We aimed to investigate the effect of maternal and postnatal high LA (HLA) diet on plasma FA composition, plasma and hepatic lipids and genes involved in lipid metabolism in the liver of adult offspring. Female rats were fed with low LA (LLA; 1.44% LA) or HLA (6.21% LA) diets for 10 weeks before pregnancy, and during gestation/lactation. Offspring were weaned at postnatal day 25 (PN25), fed either LLA or HLA diets and sacrificed at PN180. Postnatal HLA diet decreased circulating total n-3 PUFA and alpha-linolenic acid (ALA), while increased total n-6 PUFA, LA and arachidonic acid (AA) in both male and female offspring. Maternal HLA diet increased circulating leptin in female offspring, but not in males. Maternal HLA diet decreased circulating adiponectin in males. Postnatal HLA diet significantly decreased aspartate transaminase (AST) in females and downregulated total cholesterol, HDL-cholesterol and triglycerides in the plasma of males. Maternal HLA diet downregulated the hepatic mRNA expression of Hmgcr in both male and female offspring and decreased the hepatic mRNA expression of Cpt1a and Acox1 in females. Both maternal and postnatal HLA diet decreased hepatic mRNA expression of Cyp27a1 in females. Postnatal diet significantly altered circulating fatty acid concentrations, with sex-specific differences in genes that control lipid metabolism in the adult offspring following exposure to high LA diet in utero. 相似文献
9.
Δ6 Desaturation of linoleic acid (18∶2 n−6) and Δ5 desaturation of dihomo-γ-linolenic acid (20∶3 n−6) were measured in liver
microsomes from genetically obese Zucker rats (fa/fa) and from their lean littermates (Fa/−). Both groups were fed a balanced
commercial diet. The rats were 6, 9 and 12 weeks old, which corresponded to stages in their active growth period. The content
of total fatty acids and n−6 polyunsaturated fatty acids in whole liver and liver microsomes was also determined in order
to ascertain how the desaturase activities measuredin vitro reflected regulation of essential fatty acid metabolismin vivo. Contrary to values obtained for Δ6 desaturation, Δ5 desaturation at nonsaturating substrate levels were lower in obese rats
than in lean controls. In contrast, at saturating substrate level, the maximal Δ5 desaturase activities were the same in both
phenotypes and they increased with age. Study of Δ5 desaturation kinetics (1/V vs 1/S) showed that Vm did not differ between 12-week-old obese and lean rats, whereas KM in obese rats was much lower than in controls, expressing the very low affinity of the enzyme for the substrate in obese
animals. The fatty acid composition of liver lipids reflected the results of desaturase activitiesin vitro. In particular, the ratios 20∶4 n−6/20∶3 n−6 were lower in obese rats than in lean rats, which can be explained by the lower
conversion of 20∶3 n−6 into 20∶4 n−6 by Δ5 desaturation. However, the total amount of 20∶4 n−6 in the whole liver did not
differ between phenotypes, whatever their age. This work presents evidence for a relationship between the changes in fatty
acid compositional data in hepatic total lipids, total lipids of liver microsomes and modifications of fatty acid desaturase
activities in the genetically obese Zucker rat. 相似文献
10.
The effects of SMP-500, a novel ACAT inhibitor, on serum lipid levels, hepatic lipid secretion rate, and hepatic lipid disposition
in rats were studied to clarify its lipid-lowering action. SMP-500 reduced the serum cholesterol level in a dose-dependent
manner in rats fed a hypercholesterolemic diet. SMP-500 also reduced hepatic free cholesterol content in addition to hepatic
total and esterified cholesterol contents. Biliary concentrations of cholesterol and bile acid were increased by SMP-500;
however, the bile flow and lithogenic index were not affected. SMP-500 increased cholesterol 7α-hydroxylase mRNA level. Therefore,
it is suggested that the increase in concentrations of cholesterol and bile acid in bile is due to both the increase of bile
acid production through the increase of cholesterol 7α-hydroxylase and the decrease of hepatic free cholesterol content. An
inhibitory effect of SMP-500 both on the cholesterol secretion and on the TG secretion from liver was observed. SMP-500 reduced
the serum TG level in sucrose-fed rats. From these results, one may hypothesize that the suppression of hepatic VLDL secretion
probably plays an important role on both cholesterol- and TG-lowering effects of SMP-500. 相似文献
11.
12.
Feeding a diet high in excess histidine (5% L-histidine) resulted in hypercholesterolemia and enlargement of the liver in
rats. To clarify the mechanism of the hypercho-lesterolemia cholesterol synthesis and degradation were followed. We found
that hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in histidine-excess diet rats was significantly higher
than in rats fed a basal diet. Incorporation of [3H]water into cholesterol of liver slices from rats fed the histidine-excess diet was higher than incorporation into liver
slices from rats fed the basal diet (expressed per liver per 100 g body weight).In vivo incorporation of [3H]water into hepatic cholesterol was also higher, but the incorporation into cholesterol of the small intestine was lower
in histidine-fed rats than in rats fed the basal diet (expressed per liver per 100 g body weight). Hepatic cholesterol 7α-hydroxylase
activity was similar in both groups. The data suggest that the hypercholester-olemia caused by histidine-excess diet appears
to be due to the stimulation of cholesterol synthesis in the liver. 相似文献
13.
Yuka Kurosaka Shuichi Machida Yoko Shiroya Hideki Yamauchi Kumiko Minato 《International journal of molecular sciences》2021,22(4)
Weight control based on dietary restriction (DR) alone can cause lipid metabolic failure and progression to fatty liver. This study aimed to investigate the effect of exercise on preventing DR-induced hepatic fat accumulation in Zucker fatty (ZF) rats by focusing on the relationship between adipose tissue lipolysis and hepatic fat uptake. Six-week-old male ZF rats were randomly assigned to obese, DR, or DR with exercise (DR + Ex) groups. The DR and DR + Ex groups were fed a restricted diet, with the latter also undergoing voluntary exercise. After 6 weeks, hepatic fat accumulation was observed in the DR group, whereas intrahepatic fat was markedly reduced in the DR + Ex group. Compared with the obese (Ob) group, the DR group exhibited 2.09-fold expression of hepatic fatty acid translocase (FAT)/CD36 proteins (p < 0.01) and 0.14-fold expression of hepatic fatty acid-binding protein (FABP)1 (p < 0.01). There were no significant differences between the DR + Ex group and the Ob group. FAT/CD36 and hepatic triglyceride (TG) expression levels were strongly positively correlated (r = 0.81, p < 0.001), whereas there was a strong negative correlation between FABP1 and hepatic TG expression levels (r = −0.65, p < 0.001). Our results suggest that hepatic fat accumulation induced by DR in ZF rats might be prevented through exercise-induced modifications in FAT/CD36 and FABP1 expression. 相似文献
14.
Ana Maria P. Lottenberg Helena C. F. Oliveira Edna R. Nakandakare Eder C. R. Quintão 《Lipids》1992,27(5):326-330
The mechanism by which ω3 fatty acids lower plasma triacylglycerol levels was investigated. Rats were fed fish oil, olive
oil (10% fat by weight) or a nonpurified diet 4% fat by weight) for 15 days. Lipoprotein lipase was inhibited by intra-arterial
administration of Triton WR 1339 to estimate hepatic triacylglycerol output. Rats fed the olive oil diet showed a higher rate
of triacylglycerol formation than rats fed the ω3 fatty acid diet or the low-fat diet. All three groups showed identical rates
of removal from plasma of intraarterially administered artificial chylomicrons that had simultaneously been labeled with cholesteryl
[1-14C]oleate and [9,10(n)-3H]triolein. Liver radioactivity and total fat content were lowest in rats fed the fish oil diet, indicating that ω3 fatty
acids were preferentially metabolized in liver. Chylomicrons obtained from donor rats fed either fish oil containg [14C]cholesterol or olive oil containing [3H]cholesterol were removed at similar rates when infused together intraarterially into recipient animals. A slower formation
of plasma very low density lipoprotein triacylglycerols in rats fed fish oil is probably due to a faster rate of oxidation
of the fatty acid chains in the liver resulting in decreased plasma triacylglycerol concentrations. 相似文献
15.
Jean Paul Blond Georges Durand Jean Bézard 《Journal of the American Oil Chemists' Society》1998,75(2):269-274
The effect of low levels of dietary arachidonic acid (20:4n-6) on Δ6 desaturation of linoleic acid (18:2n-6) and α-linolenic
acid (18:3n-3), and on Δ5 desaturation of dihomo-γ-linolenic acid (20:3n-6) were studied in liver microsomes of obese Zucker
rats, in comparison with their lean littermates. Fatty acid composition of serum total lipids and of phospholipids from liver
microsomes and from total heart and kidney was determined to see whether modifications of desaturation rate, if any, were
reflected in the tissue fatty acid profiles. Animals fed for 12 wk on a balanced diet, containing 20:4n-6 and 18:2n-6, were
compared to those fed 18:2n-6 only. The low amount of dietary 20:4n-6 greatly inhibited Δ6 desaturation of 18:2n-6 and Δ5
desaturation of 20:3n-6, whereas Δ6 desaturation of 18:3n-3 was slightly increased in obese rats. Inhibition of the biosynthesis
of long-chain n-6 fatty acids by dietary arachidonic acid was only slightly reflected in the 20:4n-6 content of liver microsome
phospholipids. On the contrary, the enrichment of serum total lipids and heart and kidney phospholipids in this fatty acid
was pronounced, more in obese than in lean animals. Our results show that, although the desaturation rate of the n-6 fatty
acids in liver microsomes was greatly decreased by the presence of arachidonic acid in the diet, the tissue phospholipid content
in arachidonic acid was not depressed. The potentiality of synthesis of eicosanoids of the 2 family from this fatty acid is
consequently not lower, especially in obese rats, in which certain tissues are deficient in arachidonic acid, in comparison
with their lean littermates. 相似文献
16.
We investigated the influence of an egg-enriched diet on plasma, hepatic and fecal lipid levels and on gene expression levels
of transporters, receptors and enzymes involved in cholesterol metabolism. Sprague–Dawley rats fed an egg-enriched diet had
lower plasma triglycerides, total cholesterol, low density lipoprotein (LDL)-cholesterol, hepatic triglyceride, and cholesterol
concentrations, and greater plasma high-density lipoprotein cholesterol concentration, fecal neutral sterol and bile acid
concentrations than those fed a plain cholesterol diet. Chicken egg yolk had no effect on sterol 12α-hydroxylase and sterol
27α-hydroxylase; but upregulated mRNA levels of hepatic LDL-receptor, cholesterol 7α-hydroxylase (CYP7A1) and lecithin cholesterol
acyltransferase, and downregulated hepatic hydroxymethylglutaryl-(HMG)-CoA reductase and acyl-CoA:cholesterol acyltransferase
(ACAT) after 90 days. Modification of the lipoprotein profile by an egg-enriched diet was mediated by reducing de novo cholesterol
synthesis and enhancing the excretion of fecal cholesterol, via upregulation of CYP7A1 and the LDL receptor, and downregulation
of HMG-CoA reductase and ACAT. 相似文献
17.
The effect of simvastatin, a hypocholesterolemic drug, on the biosynthesis of arachidonic acid was studied in obese and lean
Zucker rats. After administration of 2 mg/kg body weight/d for 13 d, Δ6 and Δ5 desaturase activities were measured in liver
microsomes at two substrate concentrations. In untreated rats, the Δ6 desaturation rate was similar in the obese and lean
rats when measured at saturating substrate levels, whereas Δ5 desaturation was lower in the obese animals. Treatment with
simvastatin did not change Δ6 desaturation in either phenotype but increased Δ5 desaturation in obese rats to reach the unchanged
rate observed in lean animals. The changes were not reflected in the fatty acid composition of liver microsomal phospholipids
when expressed as μg fatty acid/g of liver. 相似文献
18.
Young adult obese Zucker rats have altered tissue fatty acid (FA) composition. The present study was aimed at determining
whether such changes were seen in either liver, serum or adipose tissue obtained from 17-day-old obese (fafa) rats in comparison
to both homozygous (FaFa) and heterozygous (Fafa) lean rats. Body weights of obese pups (30.3 g) were significantly greater
than those of homozygous lean rats (25.2 g) (P<0.05). Liver weight and lipid content were similar in all groups. Inguinal fat pad weight and lipid content were greatest
in obese pups (573 mg) followed by heterozygous lean pups (303 mg); homozygous lean pups (146 mg) had the lowest values. There
were no differences among the groups in hepatic FA composition in either triacylglycerol (TG) or phospholipid fractions. Serum
TG was similar among the groups, while serum phospholipid was greater (P< 0.05) in obese (269 mg/dL) than in homozygous lean pups (184 mg/dL); heterozygous lean pups had an intermediate value not
significantly different from either homozygous group. On a percent basis, there were no differences in FA composition in either
serum lipid fraction among the three groups. There were a number of significant differences in adipose tissue FA composition
between the groups on a percent basis. The adipose tissue FA composition on a percent basis reflected that of maternal milk.
The results indicate that suckling obese Zucker rats do not have tissue FA profiles that are characteristic of essential FA
deficiency. 相似文献
19.
The impact of a moderate Zn deficiency on growth and plasma and liver lipids was investigated in two 4-week experiments with
male weanling rats fed fat-enriched diets. Semisynthetic, approximately isocaloric diets containing 3% soybean oil were supplemented
with either 7 or 100 mg Zn/kg diet and with 22% beef tallow (BT) or sunflower oil (SF). In Experiment 1, which compared the
dietary fat level and the fat source in a factorial design of treatments, all diets were fed ad libitum to 6 × 8 animals,
whereas intake of the high-Zn BT and SF diets was restricted in Experiment 2 (5 × 6 rats) to the level of intake of the respective
low-Zn diets. The low-Zn SF diet consistently depressed food intake and final live weights of the animals to a greater extent
than the other low-Zn diets, while intake and growth were comparable among the animals fed the high-Zn diets. The marginal
Zn deficit per se did not alter plasma triglyceride and cholesterol concentrations nor hepatic concentrations of triglyceride,
cholesterol and phospholipids. The fatty acid pattern of liver phospholipids did not indicate that chain elongation and desaturation
of fatty acids was impaired by a lack of zinc. It was concluded that dietary energy and fat intake, and fat source have a
greater effect on plasma and liver lipids than a moderate Zn deficiency. Marginally Zn-deficient diets enriched with sunflower
oil as a major energy source cause a greater growth retardation than diets rich in carbohydrates or beef tallow. 相似文献
20.
High free fatty acid (FFA) levels are common in obesity and in diseases such as diabetes that are associated with the obese
state. Dehydroepiandrosterone (DHEA) decreases dietary fat consumption, body fat content, and insulin levels in the obese
Zucker rat (ZR), a genetic model of human youth-onset obesity and type 2 diabetes mellitus. This study was conducted to investigate
the effects of DHEA on lean and obese ZR serum, adipose, and hepatic tissue fatty acid (FA) profiles and serum FFA levels.
Because DHEA is known to decrease fat consumption and body fat, we postulate that DHEA may also alter FA profiles and FFA
levels of the obese ZR such that they more closely resemble the profiles and levels of their lean siblings. In this study
there was a DHEA and a pair-fed (PF) group (n=6) for 12 lean and 12 obese ZR. The diet of the treatment groups was supplemented with 0.6% DHEA, and PF groups were given
the same average calories consumed by their corresponding DHEA group for 30 d. Fasted animals were sacrificed, and FA profiles
and FFA levels were measured. Serum FFA levels were higher in obese (∼1 mmol/L) compared to lean rats (∼0.6 mmol/L). After
30 d of DHEA treatment, FFA levels were lower (P<0.05) in both lean and obese groups. Although several significant differences in FA profile of serum, hepatic, and adipose
lipid components were observed between lean and obese ZR, DHEA-related changes were only observed in the serum phospholipid
(PL) and liver PL and triglyceride fractions. The slight but significant decrease in serum FFA levels may be reflected by
changes in serum PL FA profiles. Specific hepatic FA profile alterations may be related to DHEA's known effects in inducing
hepatic peroxisomes. We speculate that such FA changes may give insight into a mechanism for the action of DHEA. 相似文献