Fat Depot Weights Research Articles

Influence of a rumen-protected conjugated linoleic acid mixture on carcass traits and meat quality in young simmental heifers

The aim of the present study was to investigate the influence of feeding rumen-protected CLA during the early growing period on physical and chemical beef properties in young Simmental heifers. A total of 36 heifers (5 mo old; initial BW 185 ± 21 kg) were fed 250 g of different rumen-protected fats daily for 16 wk in 1 of 3 treatment groups: 250 g of a CLA-free control fat; 100 g of a CLA fat containing 2.4% of cis-9,trans-11 CLA and 2.1% of trans-10,cis-12 CLA and 150 g control fat; or 250 g of the CLA fat. Heifer growth performance variables as well as carcass weight, classification (conformation and fatness), and weights of organs and fat depots were not affected (P > 0.05) by CLA supplementation. Concentration of trans-10,cis-12 CLA in tissues (LM and subcutaneous fat) was dose-dependently increased (P < 0.01) by CLA supplementation, whereas that of cis-9,trans-11 CLA in these tissues did not differ (P > 0.05) between groups. The ratio of SFA to MUFA was increased (P < 0.01) in tissues of CLA-fed heifers compared with control heifers. Concentration of α-tocopherol in LM was greater (P = 0.01) in heifers of the 2 CLA groups than in control heifers. Other quality characteristics such as drip loss during storage, cooking loss, intramuscular fat content, and color variables in LM did not differ (P > 0.05) between groups. In conclusion, the present study demonstrates that feeding rumen-protected CLA during the early growing period changes tissue fatty acid composition but does not influence beef quality variables. Performance variables and carcass traits in young heifers, unlike in pigs and laboratory animals, are not influenced by CLA feeding.

Differences in triglyceride and cholesterol metabolism and resistance to obesity in male and female vitamin D receptor knockout mice

A lean phenotype has been detected in vitamin D receptor (VDR) knockout mice; however, the gender differences in fat metabolism between male and female mice both with age and in response to a high-fat diet have not been studied before. The objective of our study was to assess changes in body and fat tissue weight, food intake and serum cholesterol and triglyceride in VDR knockout mice from weaning to adulthood and after a challenge of adult animals with a high-fat diet. Although VDR knockout mice of both sexes consumed more food than wild-type and heterozygous littermates, their body weight and the weight of fat depots was lower after 6 months on a diet with 5% crude fat content. When adult animals were challenged with a high-fat diet containing 21% crude fat content for 8 weeks, VDR knockout mice of both sexes had a significantly higher food intake but gained less weight than their wild-type littermates. Cholesterol levels were higher after 2 days on the high-fat diet in both sexes, but in the VDR knockout mice, less cholesterol was detected in the serum after 8 weeks. Wild-type male mice showed signs of fatty liver disease at the end of the experiment, which was not detected in the other groups. In conclusion, lack of the VDR receptor results in reduced fat accumulation with age and when adult mice are fed a high-fat diet, despite a higher food intake of VDR knockout mice relative to their wild-type littermates. These effects can be detected in both sexes. Wild-type male mice react with the highest weight gain and cholesterol levels of all groups and develop fatty liver disease after 8 weeks on a high-fat diet, while male VDR knockout mice appear to be protected.

Ultrasound imaging, biochemical blood analyses, and weight investigations of dissectible fat depots in New Zealand white rabbits

The purpose of the present study was to evaluate changes in real-time ultrasound imaging traits and weight of dissectible fat depots (inguinal, interscapular, and perirenal) in rabbits with different body weights and to monitor the changes in blood glucose and constituents of lipid profiles. In this study, 18 clinically healthy male New Zealand white rabbits were used. The rabbits were fed with standard diet and were divided into 3 groups according to their body weight: group 1 at 1.06 ± 0.03 kg, group 2 at 2.1 ± 0.05 kg, and group 3 at 3.06 ± 0.03 kg. Examined by ultrasonography, the inguinal and interscapular fat depots appeared as bands with weak to moderate echogenicity, whereas perirenal fat was moderate to hyperechoic. The thickness of subcutaneous fat depots measured by ultrasound increased along with body weight and differences between the groups were found to be statistically significant (P < 0.001). The differences in perirenal fat thickness between rabbits from group 1 and group 2 were not found to be statistically significant. Perirenal fat thickness in the rabbits from group 3 was higher (P < 0.001) than that of the other groups. Perirenal fat weight in group 3 correlated positively (r = 0.82; P < 0.05) to body weight. Blood biochemical analysis showed that blood glucose, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were in the reference range for all groups regardless of the fact that TG and HDL-C in groups 2 and 3 were significantly higher than those in rabbits from group 1. The in vivo ultrasound screening of adipose tissue, together with blood lipid profile, is an indicator of good health and proper energy balance in rabbits bred for meat or as companion animals.

Contrasting apoptotic responses of conjugated linoleic acid in the liver of obese Zucker rats fed palm oil or ovine fat

We hypothesized that reducing weight properties of conjugated linoleic acid (CLA) are due to adipocyte apoptosis and that CLA differentially modulates the apoptotic responses in hepatic lipotoxicity from rats fed saturated fat diets. Obese Zucker rats were fed atherogenic diets (2% w/w of cholesterol) formulated with high (15% w/w) saturated fat, from vegetable or animal origin, supplemented or not with 1% of a mixture (1:1) of cis-9, trans-11 and trans-10, cis-12 CLA isomers for 14 weeks. CLA induced no changes on retroperitoneal fat depot weight, which was in line with similar levels of apoptosis. Interestingly, CLA had a contrasting effect on cell death in the liver according to the dietary fat. CLA increased hepatocyte apoptosis, associated with upregulation of Fas protein in rats fed palm oil, compared to rats receiving palm oil alone. However, rats fed ovine fat alone displayed the highest levels of hepatic cell death, which were decreased in rats fed ovine fat plus CLA. This reducing effect of CLA was related to positively restoring endoplasmic reticulum (ER) ATF-6α, BiP and CHOP protein levels and increasing phosphorylated c-Jun NH 2-terminal kinase (JNK) and c-Jun, thus suggesting an adaptive response of cell survival. These findings reinforce the role of CLA as regulator of apoptosis in the liver. Moreover, the dietary fat composition is a key factor in activation of apoptosis.

Maternal high-fat feeding through pregnancy and lactation predisposes mouse offspring to molecular insulin resistance and fatty liver

The exposure to an increased supply of nutrients before birth may contribute to offspring obesity. Offspring from obese dams that chronically consume a high-fat diet present clinical features of metabolic syndrome, liver lipid accumulation and activation of c-Jun N-terminal kinases (JNK) consistent with the development of nonalcoholic fatty liver disease (NAFLD). However, in spite of the importance of the resistance to insulin for the development of NAFLD, the molecular alterations in the liver of adult offspring of obese dams are yet to be investigated. In this study, we tested the hypothesis that the consumption of excessive saturated fats during pregnancy and lactation contributes to adult hepatic metabolic dysfunction in offspring. Adult male offspring of dams fed a high-fat diet (HN) during pregnancy and lactation exhibited increased fat depot weight; increased serum insulin, tumor necrosis factor α and interleukin 1β; and reduced serum triglycerides. Liver showed increased JNK and I kappa B kinase phosphorylation and PEPCK expression in the adult. In addition, liver triglyceride content in the offspring 1 week after weaning and in the adult was increased. Moreover, basal ACC phosphorylation and insulin signaling were reduced in the liver from the HN group as compared to offspring of dams fed a standard laboratory chow (NN). Hormone-sensitive lipase phosphorylation (Ser565) was reduced in epididymal adipose tissue from the HN group as compared to the NN group. It is interesting that all changes observed were independent of postweaning diet in 14-week-old offspring. Therefore, these data further reinforce the importance of maternal nutrition to adult offspring health.

Maternal Omega-3 Supplementation Increases Fat Mass in Male and Female Rat Offspring

Adipogenesis and lipogenesis are highly sensitive to the nutritional environment in utero and in early postnatal life. Omega-3 long chain polyunsaturated fatty acids (LCPUFA) inhibit adipogenesis and lipogenesis in adult rats, however it is not known whether supplementing the maternal diet with omega-3 LCPUFA results in reduced fat deposition in the offspring. Female Albino Wistar rats were fed either a standard chow (Control, n = 10) or chow designed to provide ∼15 mg/kg/day of omega-3 LCPUFA, chiefly as docosahexaenoic acid (DHA), throughout pregnancy and lactation (Omega-3, n = 11) and all pups were weaned onto a commercial rat chow. Blood and tissues were collected from pups at 3 and 6 weeks of age and weights of visceral and subcutaneous fat depots recorded. The expression of adipogenic and lipogenic genes in the subcutaneous and visceral fat depots were determined using quantitative real time reverse transcription-PCR. Birth weight and postnatal growth were not different between groups. At 6 weeks of age, total percentage body fat was significantly increased in both male (5.09 ± 0.32% vs. 4.56 ± 0.2%, P < 0.04) and female (5.15 ± 0.37% vs. 3.89 ± 0.36%, P < 0.04) offspring of omega-3 dams compared to controls. The omega-3 LCPUFA content of erythrocyte phospholipids (as a% of total fatty acids) was higher in omega-3 offspring (6.7 ± 0.2% vs. 5.6 ± 0.2%, P < 0.001). There was no effect of maternal omega-3 LCPUFA supplementation on the expression of adipogenic or lipogenic genes in the offspring in either the visceral or subcutaneous fat depots. We have therefore established that an omega-3 rich environment during pregnancy and lactation in a rodent model increases fat accumulation in both male and female offspring, particularly in subcutaneous depots, but that this effect is not mediated via upregulation adipogenic/lipogenic gene transcription. These data suggest that maternal n−3 LCPUFA supplementation during pregnancy/lactation may not be an effective strategy for reducing fat deposition in the offspring.

Dietary saturated fat/cholesterol, but not unsaturated fat or starch, induces C-reactive protein associated early atherosclerosis and ectopic fat deposition in diabetic pigs.

BackgroundDiabetes is thought to accelerate cardiovascular disease depending on the type of diet. This study in diabetic subjects was performed to investigate the metabolic, inflammatory and cardiovascular effects of nutritional components typically present in a Western, Mediterranean or high glycaemic diet.MethodsStreptozotocin-diabetic pigs (~45 kg) were fed for 10 weeks supplemental (40% of dietary energy) saturated fat/cholesterol (SFC), unsaturated fat (UF) or starch (S) in an eucaloric dietary intervention study.ResultsFasting plasma total, LDL and HDL cholesterol concentrations were 3-5 fold higher (p < 0.01) in SFC compared to UF and S pigs. Fasting plasma NEFA concentrations (mmol/L) were highest (p < 0.05) in SFC (1.09 ± 0.17), intermediate in UF (0.80 ± 0.14) and lowest in S pigs (0.58 ± 0.14) whereas plasma glucose (~13 mmol/L), triglyceride (~0.5 mmol/L) and insulin (~24 pmol/L) concentrations were comparable among SFC, UF and S pigs. The postprandial response area under the curves (AUC, 0-4 h) for glucose but not for insulin and triglyceride responses were intermediate in SFC (617 ± 144) and lowest (p < 0.05) in UF (378 ± 157) compared to S pigs (925 ± 139). Fasting hepatic glucose production, hepatic and peripheral insulin sensitivity and blood pressure were not different among pigs. C-reactive protein (CRP) concentrations (mg/L) were highest (p < 0.05) in SFC (25 ± 4), intermediate in S (21 ± 3) and lowest in UF pigs (14 ± 2). Liver weights, liver and muscle triglyceride concentrations, and the surface area of aorta fatty streaks were highest (p < 0.01) in SFC pigs. A positive correlation between postprandial plasma CRP and aorta fatty streaks was observed in SFC pigs (R2 = 0.95). Retroperitoneal fat depot weight (g) was intermediate in SFC (260 ± 72), lowest in S (135 ± 51) and highest (p < 0.05) in UF (571 ± 95) pigs.ConclusionDietary saturated fat/cholesterol induces inflammation, atherosclerosis and ectopic fat deposition whereas an equally high dietary unsaturated fat load does not induce these abnormalities and shows beneficial effects on postprandial glycaemia in diabetic pigs.

Diet‐Dependent Genetic and Genomic Imprinting Effects on Obesity in Mice

Although the current obesity epidemic is of environmental origin, there is substantial genetic variation in individual response to an obesogenic environment. In this study, we perform a genome-wide scan for quantitative trait loci (QTLs) affecting obesity per se, or an obese response to a high-fat diet in mice from the LG/J by SM/J Advanced Intercross (AI) Line (Wustl:LG,SM-G16). A total of 1,002 animals from 78 F₁₆ full sibships were weaned at 3 weeks of age and half of each litter placed on high- and low-fat diets. Animals remained on the diet until 20 weeks of age when they were necropsied and the weights of the reproductive, kidney, mesenteric, and inguinal fat depots were recorded. Effects on these phenotypes, along with total fat depot weight and carcass weight at necropsy, were mapped across the genome using 1,402 autosomal single-nucleotide polymorphism (SNP) markers. Haplotypes were reconstructed and additive, dominance, and imprinting genotype scores were derived every 1 cM along the F₁₆ map. Analysis was performed using a mixed model with additive, dominance, and imprinting genotype scores, their interactions with sex, diet, and with sex-by-diet as fixed effects and with family and its interaction with sex, diet, and sex-by-diet as random effects. We discovered 95 trait-specific QTLs mapping to 40 locations. Most QTLs had additive effects with dominance and imprinting effects occurring at two-thirds of the loci. Nearly every locus interacted with sex and/or diet in important ways demonstrating that gene effects are primarily context dependent, changing depending on sex and/or diet.

The effects of a high-fat, high-cholesterol diet on markers of uterine contractility during parturition in the rat

Increasing levels of obesity within women of reproductive age is a major concern in the UK. Approximately, 13% of women aged <30 and 22% of 31- to 40-year-old women are obese. Obesity increases complications during pregnancy and the risk of caesarean section due to prolonged labour and poor uterine activity. The aim was to investigate whether a high-fat, high-cholesterol (HFHC) diet decreases markers of uterine contractility during parturition in the rat. Female Wistar rats were fed control (CON, n=10) or HFHC (n=10) diets for 6 weeks. Animals were mated and, once pregnant, maintained on their diet throughout gestation. On gestational day 19, rats were monitored continuously and killed at the onset of parturition. Body and fat depot weights were recorded. Myometrial tissue was analysed for cholesterol (CHOL), triglycerides (TAG), and expression of the contractile associated proteins gap junction protein alpha 1 (GJA1; also known as connexin-43, CX-43), prostaglandin-endoperoxide synthase 2 (PTGS2; also known as cyclo-oxygenase-2, COX-2) and caveolin-1 (CAV1) and maternal plasma for prostaglandin F(2)(α) (PGF(2)(α)) and progesterone. HFHC fed rats gained greater weight than CON (P<0.003) with significant increases in peri-renal fat (P<0.01). The HFHC diet increased plasma CHOL, TAG and progesterone, but decreased PGF(2)(α) versus CON (P<0.01, P<0.01, P=0.05 and P<0.02 respectively). Total CHOL and TAG levels of uterine tissue were similar. However, HFHC fed rats showed significant increases in PTGS2 (P<0.037), but decreases in GJA1 and CAV1 (P=0.059). In conclusion, a HFHC diet significantly increases body weight and alters lipid profiles that correlate with decreases in key markers of uterine contractility. Further work is required to ascertain whether these changes have adverse effects on uterine activity.

Glucosamine attenuates increases of intraabdominal fat, serum leptin levels, and insulin resistance induced by a high-fat diet in rats

The levels of circulating nonesterified fatty acids increase during obesity and contribute to insulin resistance by inhibiting insulin-stimulated glucose transport and phosphorylation in human muscles. In cells, glucose-6-phosphate is primarily used in glycogenesis and glycolysis; only 1% to 3% is converted to glucosamine-6-phosphate, which enters the hexosamine-biosynthesis pathway. The major end product of this pathway, uridine-5'-diphosphate-N-acetyl-glucosamine, which is increased by exogenous glucosamine (GlcN) administration, mediates insulin resistance. We hypothesized that the administration of GlcN to rats receiving a high-fat (HF) diet may potentiate the effects of an HF diet on glucose tolerance and other metabolic variables. To evaluate this relationship, 2 groups of rats were fed with a control or HF diet; and another 2 groups received glucosamine hydrochloride at a dose of 500 mg/kg dissolved in drinking water for 21 weeks. Metabolic variables related to insulin resistance were then measured. The levels of blood glucose and serum insulin were higher in a glucose tolerance test in the HF group as compared with the control group. Rats receiving GlcN had reduced liver glycogen and only slightly worsened glucose tolerance as compared with control rats, although this did not induce insulin resistance as evaluated by the homeostasis model assessment. Glucosamine administration was able to partially or completely inhibit some effects of the HF diet by reducing fat depot weight and serum leptin levels, thus resulting in a smaller increase in the insulinemic response to a glucose injection and lower postabsorptive glycemia.

Adipose Acyl-CoA Synthetase-1 Directs Fatty Acids toward β-Oxidation and Is Required for Cold Thermogenesis

Long-chain acyl-CoA synthetase-1 (ACSL1) contributes 80% of total ACSL activity in adipose tissue and was believed to be essential for the synthesis of triacylglycerol. We predicted that an adipose-specific knockout of ACSL1 (Acsl1(A-/-)) would be lipodystrophic, but compared to controls, Acsl1(A-/-) mice had 30% greater fat mass when fed a low-fat diet and gained weight normally when fed a high-fat diet. Acsl1(A-/-) adipocytes incorporated [(14)C]oleate into glycerolipids normally, but fatty acid (FA) oxidation rates were 50%-90% lower than in control adipocytes and mitochondria. Acsl1(A-/-) mice were markedly cold intolerant, and beta(3)-adrenergic agonists did not increase oxygen consumption, despite normal adrenergic signaling in brown adipose tissue. The reduced adipose FA oxidation and marked cold intolerance of Acsl1(A-/-) mice indicate that normal activation of FA for oxidation in adipose tissue in vivo requires ACSL1. Thus, ACSL1 has a specific function in directing the metabolic partitioning of FAs toward beta-oxidation in adipocytes.

The Effect of Mannan Oligosaccharide Supplementation on Body Weight Gain and Fat Accrual in C57Bl/6J Mice

The prevalence of obesity in industrialized societies has become markedly elevated. In contrast, model organism research shows that reducing caloric intake below ad libitum levels provides many health and longevity benefits. Despite these benefits, few people are willing and able to reduce caloric intake over prolonged periods. Prior research suggests that mannooligosaccharide (MOS or mannan) supplementation can increase lifespan of some livestock and in rodents can reduce visceral fat without reducing caloric intake. Hence, we tested the effect of MOS supplementation as a possible calorie restriction (CR) mimetic (CRM) in mice. C57Bl/6J male mice were fed a high-fat "western" type diet with or without 1% MOS (by weight) supplementation (n = 24/group) from 8 to 20 weeks of age. Animals were housed individually and provided 95% of ad libitum food intake throughout the study. Body weight was measured weekly and body composition (lean and fat mass) measured noninvasively every 3 weeks. Individual fat depot weights were acquired by dissection at study completion. Supplementation of a high-fat diet with 1% MOS tended to reduce total food intake (mean +/- s.d.; control (CON): 293.69 +/- 10.53 g, MOS: 288.10 +/- 11.82 g; P = 0.09) during the study. Moreover, MOS supplementation had no significant effect on final body weight (CON: 25.21 +/- 2.31 g, MOS: 25.28 +/- 1.49 g; P = 0.91), total fat (CON: 4.72 +/- 0.90 g, MOS: 4.82 +/- 0.83 g; P = 0.69), or visceral fat (CON: 1.048 +/- 0.276 g, MOS: 1.004 +/- 0.247 g; P = 0.57). Contrary to previous research, MOS supplementation had no discernable effect on body weight gain or composition during this 12-week study, challenging the potential use of MOS as a CRM or body composition enhancer.

Obesity induced by cafeteria feeding and pregnancy outcome in the rat

Obesity during pregnancy has major consequences for maternal and neonatal health, but the long-term effects on the offspring are less clear. It is not known whether the effects observed in animal models are a result of maternal obesity per se or of the high-fat diets used to induce obesity. This investigation aimed to develop a model for the evaluation of the independent effects of cafeteria feeding and maternal obesity, considering their impact on plasma volume expansion, circulating metabolites, and fetal and placental growth. Wistar rats were fed a control or cafeteria diet from weaning. After 8 weeks, all animals were mated and half of the animals within each group were crossed-over to the alternative diet. This generated four treatment groups, differing in their pre-gestational and gestational diets. Half of the animals were culled at day 5 of gestation and the remainder at day 20. Maternal body composition, blood volume and circulating glucose, TAG and cholesterol were determined. Cafeteria feeding was effective in inducing obesity, as demonstrated by increased fat depot weights and total body fat, without impacting upon reproductive success or circulating lipid concentrations. The study successfully demonstrated that there were differential effects of maternal body fatness and diet upon fetal and placental growth, with pre-gestational obesity leading to lower fetal weight at day 20 of gestation (P < 0.001). The model will provide a useful vehicle for the investigation of the complex interactions between dietary- and obesity-related factors during pregnancy in their effects on fetal development and postnatal metabolic function.

The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation

We investigated the role of LMNA in adipose tissue by developing a novel mouse model of lipodystrophy. Transgenic mice were generated that express the LMNA mutation that causes familial partial lipodystrophy of the Dunnigan type (FPLD2). The phenotype observed in FPLD-transgenic mice resembles many of the features of human FPLD2, including lack of fat accumulation, insulin resistance, and enlarged, fatty liver. Similar to the human disease, FPLD-transgenic mice appear to develop normally, but after several weeks they are unable to accumulate fat to the same extent as their wild-type littermates. One poorly understood aspect of lipodystrophies is the mechanism of fat loss. To this end, we have examined the effects of the FPLD2 mutation on fat cell function. Contrary to the current literature, which suggests FPLD2 results in a loss of fat, we found that the key mechanism contributing to the lack of fat accumulation involves not a loss, but an apparent inability of the adipose tissue to renew itself. Specifically, preadipocytes are unable to differentiate into mature and fully functional adipocytes. These findings provide insights not only for the treatment of lipodystrophies, but also for the study of adipogenesis, obesity, and insulin resistance.

Effect of high-fat diet feeding on leptin receptor expression in white adipose tissue in rats: depot- and sex-related differential response

Previous studies have illustrated the importance of leptin receptor (OB-Rb) mediated action on adipocytes in the regulation of body weight. The aim of the present study was to investigate in male and female rats the effects of high-fat (HF) diet feeding on the expression levels of OB-Rb in different depots of white adipose tissue (WAT), and its relation to fatty acid oxidation capacity. Male and female Wistar rats were fed until the age of 6 months with a normal-fat (NF) or non-isocaloric HF-diet (10 and 45% calories from fat, respectively). At this age, the weight of three different fat depots (retroperitoneal, mesenteric and inguinal) and the expression levels of OB-Rb, PPARalpha and CPT1 in these depots were measured. HF-diet feeding resulted in an increase in the weight of the different fat depots, the retroperitoneal depot being the one with the greatest increase in both sexes. In this depot, HF-diet feeding resulted in a significant decrease in OB-Rb mRNA levels, more marked in male than in female rats. In the mesenteric depot, the effects of HF-diet feeding on OB-Rb mRNA levels were sex-dependent: they decreased in males rats (associated with a decrease in PPARalpha and CPT1 mRNA levels), but increased in female rats. In the inguinal depot, OB-Rb expression was not affected by HF-diet feeding. These results show that a chronic intake of an HF-diet altered the expression of OB-Rb in WAT in a depot and sex-dependent manner. The decreased expression of OB-Rb in the internal depots of male rats under HF-diet feeding, with the resulting decrease in leptin sensitivity, can help to explain the higher tendency of males to suffer from obesity-linked disorders under HF-diet conditions.

Diet supplementation with the cis-9,trans-11 conjugated linoleic acid isomer affects the size of adipocytes in Wistar rats

Previous reports have demonstrated that conjugated linoleic acid (CLA) acts on body fat accumulation in a variety of animal models. The aim of the present study was to investigate the effect of cis (c)-9,trans (t)-11 and t10,c12 CLA isomers on the number and size of adipocytes from the inguinal and retroperitoneal fats in Wistar male rats. A 5.1% palm oil-based diet was supplemented with CLA isomers as follows: 0.6% of c9,t11, 0.6% of t10,c12, 1.3% of c9,t11 and t10,c12 isomers in mixture, and a control nonsupplemented group for comparative purposes. Fat tissues were prepared on microscope slides for histologic examination using an image-analysis software to count the number of adipocytes and measure cell sizes. The results showed that CLA isomers did not affect (P > .05) either final body and fat depot weights or serum lipids (with the exception of triacylglycerols) and adipocytokines (leptin and adiponectin). Animals fed the c9,t11 CLA isomer diet showed larger adipocytes when compared to other groups. Independently of the CLA dietary treatment, retroperitoneal fat showed larger adipocytes (3319 microm(2)) and therefore a smaller number of adipocytes per unit of area, compared to inguinal fat (3055 microm(2)). Taken together, the data suggest that a palm oil-based diet supplemented with the c9,t11 CLA isomer in Wistar rats, in contrast to the t10,c12 isomer and the mixture of both isomers, increases adipocyte dimensions in inguinal and retroperitoneal fat depots, while having a minor effect in serum lipids and adipocytokines.

Liver of ovariectomized rats is resistant to resorption of lipids

Ovarian hormones have been shown to regulate liver lipid accumulation in rats. The present study was designed to evaluate liver lipid resorption in ovariectomized (Ovx) rats. Ovx and sham-operated (Sham) rats were submitted to a high-fat (HF; 43% kcal fat as energy) diet for 5 weeks and then either maintained on this diet or switched to a standard (SD; 12.5% kcal fat as energy) diet till weeks 8 and 13 ( n = 8 rats/group). Body weight, energy intake, liver and intra-abdominal fat accumulation and plasma metabolic profile were determined. Body weight was significantly ( P < 0.01) higher in Ovx than in Sham groups at all times and switching diet did not alter the body weight pattern. The weight of the intra-abdominal fat depots and plasma leptin levels, along with liver triacylglycerol (TAG) concentrations, were significantly higher ( P < 0.01) in Ovx than in Sham rats. Switching diet reduced intra-abdominal fat depot weight and plasma leptin in all groups. Switching diet also resulted in a decrease in liver fat accumulation in Sham rats at all times. However, 8 weeks after the diet switch (week 13) liver fat accumulation was as high in Ovx rats as those maintained on the HF diet. When liver TAG values measured at week 13 were compared to initial pre-switching values (week 5), liver TAG levels in Ovx animals were maintained at the same level independently of the diet switch, while in Sham rats switching to a SD diet reduced liver TAG accumulation ( P < 0.05). The same comparisons with plasma TAG levels revealed an opposite relationship. These data suggest that liver lipid resorption in Ovx animals is more related to the ovarian hormone status than to the type of ingested diet.

In vivo estimation of goat carcass composition and body fat partition by real-time ultrasonography

The accuracy of ultrasound measurements to assess goat carcass composition and the partition of body fat depots was evaluated. An ultrasound machine with a 5-MHz probe and image analysis was used to assess in vivo fat thickness and muscle depth in 56 Spanish Celtiberica adult goats, in lumbar and breast body regions. The goats were slaughtered and the weight of body fat depots recorded. Measurements corresponding to the in vivo ultrasound fat thickness and muscle depth were taken on carcasses. The left sides of carcasses were completely dissected into their components. The best relationships (r = 0.94, P < 0.01) between in vivo and carcass measurements of fat thickness were obtained when measurements were taken at the sternum, and the best anatomical point was located between the third and fourth sternebrae. The best correlation coefficients (r = 0.84) for muscle depth were found for measurements taken between the third and the fourth lumbar vertebrae at 2 cm from the middle of the vertebral column. Body weight and ultrasound measurements were used to fit the best multiple regression equations to predict carcass composition and the partition of body fat depots. All equations, with the exception of those for muscle quantity, omental, and total body fat depot amounts, were computed after performing a logarithmic transformation. Body weight in association with the ultrasound measurement taken at largest LM muscle depth, between the first and second lumbar vertebrae accounted for 90% of the muscle weight. Body weight was the first variable admitted into the prediction models of muscle, mesenteric fat, and total body fat and accounted for 82, 67, and 79% of the variation in tissue weights, respectively. The ultrasound measurement of fat thickness taken at the third sternebra was the first variable admitted into the prediction models for intermuscular fat, kidney and pelvic fat, and total carcass fat and accounted for by 73, 75, 71, and 79% of the variation in the weight of these fat depots, respectively. The ultrasound measurements taken in the breast region, particularly at the third and fourth sternebrae, were the most suitable for assessing fat thickness. The results of this experiment suggest that BW associated with some in vivo ultrasonic fat measurements allow the accurate prediction of goat carcass composition and body fat depots.

Metabolic Characteristics of Wistar Rats Submitted to High Fructose Ingestion by Different Protocols

PURPOSE: Although the fructose-fed rat model exhibits many signals of the metabolic syndrome, the alterations observed are quite divergent among the studies. In search of an adequate animal model for the study of the effects of exercise on the development of the metabolic syndrome, the present study was designed to analyze metabolic characteristics of Wistar rats submitted to high fructose ingestion by different protocols. METHODS: In the first, two groups of adult rats (90 days old) were studied: a Control group (C 1; n = 6) received regular rodent chow and a Fructose group (F1; n= 6) was fed regular rodent chow and fructose was administered as a 10% solution in drinking water. In the second, also two groups of adult rats (90 days old) were evaluated: a Control group (C2; n = 6) was fed a balanced diet (AIN93) and a fructose group (F2; n= 6) was fed a purified 60% fructose diet. In the third, two groups of young rats (28 days old) were analyzed: a Control group (C3; n = 6) was fed the balanced AIN93 diet and a fructose diet group (F3; n= 6) was fed the 60 % fructose diet. The animals were evaluated with respect to: glucose tolerance (area under serum glucose concentrations during oral glucose tolerance test), peripheral insulin sensivity (serum glucose disappearance rates during subcutaneous insulin tolerance test), serum triglycerides concentration and mesenteric fat depot weight. C3 and F3 rats were also evaluated with respect to the aerobic capacity (maximal lactate steady state determination during swimming) RESULTS: Glucose tolerance was lower in the fructose groups F2 (10%) and F3 (10.4%) whereas serum triglycerides were higher (F2=99%, F3=60.2%) than in the respective controls (t- student P< 0.05). Insulin sensivity in F2 decreased (35.6%) and mesenteric fat depot weight increased (56.6%) in relation to C2. High fructose intake (F3) did not alter the aerobic capacity of the animals. CONCLUSIONS: In conclusion, high fructose intake is more effective in producing signals of metabolic syndrome in adult (90 days old) than in young (28 days old) Wistar rats. Also diet seems to be a more effective route for fructose administration than drinking water. Supported by Fapesp: process 07/54098-0; Capes and CNPq

Sex‐differential Expression of Metabolism‐related Genes in Response to a High‐fat Diet

The aim of this work was to determine the sex-associated differences in the expression of genes related to lipid metabolism and fuel partitioning in response to a high-fat (HF) diet in rats, and whether this is linked to the higher tendency of males to suffer from metabolic disorders. Male and female Wistar rats were fed for 6 months on a normal-fat (NF) or an HF diet. Body weight, fat depot weight, lipid concentration in liver, blood metabolites, and the expression of genes involved in fuel metabolism and partitioning in the liver, white adipose tissue (WAT), and skeletal muscle were measured. Female rats fed on an HF diet gained more weight and had a greater increase in the adiposity index than male rats, while the circulating insulin levels remained unaltered; these animals also showed an increased expression of genes related to the energy influx in WAT and with fat utilization in skeletal muscle. Male but not female rats showed increased hepatic peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and CPT1L mRNA expression, suggesting enhanced lipid handling and oxidation by this organ, and have a higher triacylglycerol content in liver. Male rats under the HF diet also displayed higher blood insulin levels. These results show sex-dependent differences in lipid handling and partitioning between tissues in response to an HF diet, with females showing a higher capacity for storing fat in adipose tissue and for oxidizing fatty acids in muscle. These adaptations can help to explain the lower tendency of females to suffer from obesity-linked disorders under the conditions of an HF diet.