Epididymal Fat Pad Weight Research Articles

Sucrose-induced obesity impairs novel object recognition learning in young rats

In addition to its metabolic consequences, obesity may lead to impairments in learning and memory. To test this possibility, male Long-Evans rats were fed ground chow, or chow and either a 32% sucrose solution or hydrogenated vegetable fat (Crisco®) for eight weeks. Cognitive behavior was then assessed using a novel object recognition task. To determine if there was a relationship between cognitive behavior and glucose metabolism, performance on the novel object recognition task was correlated with fasting blood glucose levels and responses on an oral glucose tolerance test. Rats fed sucrose or fat consumed more calories, gained more weight, and had larger epididymal fat pads than rats fed only chow. Additionally, fasting blood glucose levels, and the area under the glucose curve following an oral glucose tolerance test were greater in rats consuming a supplemental source of fat or sucrose than in those eating only chow. During training when rats were presented with two identical objects in an open field, time spent exploring the objects did not differ as a function of dietary conditions. However, when rats were tested 1 h later with one familiar and one novel object, rats given sucrose spent significantly less time exploring the novel object than rats eating only chow. The percent of time spent exploring the novel object was negatively correlated with fasting blood glucose levels, final body weights, and epididymal fat pad weights. It is hypothesized that the impairment in object recognition in rats eating sucrose is due, at least in part, to diet-induced alterations in glucose metabolism.

Tlr‐4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat

Toll-like receptor-4 (Tlr-4), a key pattern recognition receptor involved in innate immune response, is activated by saturated fatty acids (SFAs). To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr-4-deficient 10ScN mice and 10J controls. Mice were fed either low fat (low-fat control (LFC)), high unsaturated fat (high-fat control (HFC)), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Relative to the LFC diet, the HFC diet resulted in greater epididymal fat pad weights and adipocyte hypertrophy in both Tlr-4-deficient and normal mice. However, the 10ScN mice were completely protected against the obesigenic effects of the HFP diet. Moreover, macrophage infiltration and monocyte chemotactic protein-1 (MCP-1) transcript abundance were lower in adipose tissue of 10ScN mice fed the HFP diet, and the hyperinsulinemic response was negated. Tlr-4-deficient mice also had markedly lower circulating concentrations of MCP-1 and much less nuclear factor-kappaB (NFkappaB) protein in nuclear extracts prepared from adipose tissue, irrespective of diet. In contrast, Tlr-4 deficiency did not attenuate the induction of tumor necrosis factor-alpha (TNF-alpha) or interleukin-6 (IL-6) expression in adipose tissue. These data indicate that Tlr-4 deficiency selectively protects against the obesigenic effects of SFA and alters obesity-related inflammatory responses in adipose tissue.

Diacylglycerol consumption and blood lipids and adiposity in rats

Diacylglycerol (DAG) rich oil can promote lower adiposity and concentrations of serum triglycerides (TG) compared to triacylglycerol (TAG) rich fats. Most research, however, has assessed the influence of DAG fed at relatively high levels rather than the moderately low amounts evaluated here. Sixteen male weanling Sprague‐Dawley rats were equally divided into two groups. Rats consumed diets consisting of 21% fat by weight, mainly from coconut oil. DAG replaced 4% of the coconut oil for one group. After 30 days, serum total cholesterol (TC), HDL‐C, TG, glucose, and epididymal fat pad weights were assessed. Food intake (428 ± 46 vs. 457 ± 45 g), weight gain (184 ± 20 vs. 189 ± 15 g), food efficiency ratio (0.43 ± 0.05 vs. 0.41 ± 0.04), fat pad weights (2.740 ± 0.822 vs. 2.811 ± 0.488 g), TG (41.0 ± 20.0 vs. 51.3 ± 10.3 mg/dl), TC (78.7 ± 14.0 vs. 80.7 ± 18.8 mg/dl), and glucose (160.8 ± 31.1 vs. 169.8 ± 41.7 mg/dl) were similar (p>0.05) between the DAG and coconut oil fed rats, respectively. HDL‐C concentration (43.8 ± 6.0 vs. 56.5 ± 5.8 mg/dl) was lower for DAG‐fed rats (p<0.05). Results suggest that consuming a diet containing excess levels of saturated fat with moderately low amounts of DAG does not significantly improve lipids or reduce fat storage and may actually lower HDL‐C. Researchers should examine the minimum amount of DAG required to elicit positive responses and as a part of what type of diet the effects are most pronounced.

EDHF prevents endothelial dysfunction in response to a high‐fat diet in the Wistar rat

Individuals consuming a high‐fat diet, often display reduced responsiveness to endothelial‐dependant vasodilators such as acetylcholine or bradykinin. Endothelium‐derived hyperpolarizing factor (EDHF) may be an important vasoactive factor in resistance arteries from many vascular beds. However, its importance relative to other endothelial derived relaxing factors such as nitric oxide and prostaglandins is unclear. Although, genetic models of obesity and type II diabetes have demonstrated that EDHF‐mediated vasodilation is impaired; it is unknown if EDHF function is also affected by a high‐fat diet. 3–4 wk old Male Wistar rats were fed either a high‐fat diet (60% lard) or chow for 10–11 wks. Isolated small mesenteric arteries were pre‐constricted with Phenylephrine (PE; 10−9 – 10−5 M) and administered acetylcholine (ACh; 10−8 – 10−6 M) in the presence of either vehicle or Indomethacin (10 μm) and N(ω)‐nitro‐L‐arginine (L‐NNA; 100 μm). Vasoconstrictor responses to PE were also assessed in a separate set of untreated arteries. Blood pressure was determined by tail‐cuff. Body and epididymal fat pad weight were significantly greater in fat‐fed rats compared to chow fed. Mean arterial blood pressure was not different between groups. ACh‐induced dilation in arteries treated with vehicle was similar between chow and fat‐fed rats. Pre‐treating arteries with Indomethacin and L‐NNA blunted ACh‐mediated vasodilation in chow fed rats but did not alter ACh responses in arteries from fat‐fed animals. Reactivity to PE was not different between groups. These results suggest that role for EDHF in ACh‐mediated vasodilation is enhanced in small mesenteric arteries following a high‐fat diet.

Hydroxypropyl methylcellulose, a viscous indigestible polysaccharide, reduces adiposity and lowers plasma leptin and resistin concentrations in rats

Previous studies in this laboratory have suggested that viscous indigestible polysaccharides reduce adiposity with little or no effect on body weight. To further understand this effect, we have examined the effect of a viscous indigestible polysaccharide, hydroxypropyl methylcellulose (HPMC) on body composition and plasma adipokines in rats. Male Wistar rats were fed either a cellulose based control diet (no viscosity) (n = 12) or HPMC‐containing diet (high viscosity) (n = 24) for 6 weeks. Body composition was measured by dual X‐ray absorptiometry (DEXA) before and after 6 weeks of feeding. Rats fed the HPMC diet had a high intestinal contents viscosity whereas rat fed cellulose diet had no intestinal contents viscosity. After statistically adjusting for slight differences in final body weight, rats fed HPMC had significantly reduced body fat mass and greater lean body mass than the cellulose group, based on DEXA scanning and lower weights of epididymal and perirenal fat pads. Rats fed HPMC had significantly lower fasting plasma leptin and resistin concentrations. However, plasma adiponectin levels did not differ between the groups. There were no significant differences between groups in fasting plasma glucose or insulin levels. These results indicate that viscous indigestible polysaccharides reduce adiposity independent of an effect on body weight. (Supported by Imagenetix Inc.)

Effects of red ginseng ethanol extract on lipid metabolism in C57BL/6J mice fed high‐fat diets

This study evaluated the effects of supplementation of red ginseng ethanol extract (RG‐EtOH; 0.1%, 0.5%, and 1% of high‐fat diet) in C57BL/6J mice fed high‐fat diet (60% fat kcal) for 8 weeks. The RG‐EtOH diet groups did not show any difference in food and energy intakes compared with the high‐fat diet group, but had lower final body weights, epididymal, and back fat pad weights. Triglyceride and total cholesterol concentrations of RG‐EtOH diet groups in serum were significantly lower than high‐fat diet group. Higher concentrations of RG‐EtOH, however, did not have greater effects on serum lipid profiles. Although the 1% concentration of RG‐EtOH group had lower lipid profiles and fat pad weight than high‐fat diet group, the effect was not as great as in the 0.5 percent of RG‐EtOH. These results were confirmed by mRNA expressions of enzymes (ACS, CPT‐I, PPAR‐α, PPAR‐γ, and ACC) which are related to lipid metabolism by reverse transcriptional‐PCR. We suggest that 0.5% RG‐EtOH is the most effective dose for improving lipid metabolism. Also, our study show that red ginseng ethanol extract reduced obesity induced by high‐fat diets. (This study was supported from the KT&G Central Research Institute.)

Diet-induced obesity alters protein synthesis: tissue-specific effects in fasted versus fed mice

The influence of obesity on protein dynamics is not clearly understood. We have designed experiments to test the hypothesis that obesity impairs the stimulation of tissue-specific protein synthesis after nutrient ingestion. C57BL/6J mice were randomized into 2 groups: group 1 (control, n = 16) was fed a low-fat, high-carbohydrate diet, whereas group 2 (experimental, n = 16) was fed a high-fat, low-carbohydrate diet ad libitum for 9 weeks. On the experiment day, all mice were fasted for 6 hours and given an intraperitoneal injection of 2H 2O. They were then randomized into 2 subgroups and either given a sham saline gavage or a liquid-meal challenge. Rates of protein synthesis were determined via the incorporation of [ 2H]alanine (5 hours postchallenge) into total gastrocnemius muscle protein, total liver protein, and plasma albumin. High-fat feeding led to an increase in total body fat ( P < .001) and epididymal fat pad weights ( P < .001) and elevated fasting plasma glucose levels ( P < .01). Diet-induced obesity ( a) did not affect basal rates of skeletal muscle protein synthesis, but did impair the activation of skeletal muscle protein synthesis in response to nutrient ingestion ( P < .05), and ( b) slightly reduced basal rates of synthesis of total hepatic proteins and plasma albumin ( P = .10), but did not affect the synthesis of either in response to the meal challenge. In conclusion, there are alterations in tissue-specific protein metabolism in the C57BL/6J mouse model of diet-induced obesity. This model may prove to be helpful in future studies that explore the mechanisms that account for altered protein dynamics in obesity.

Differences in adipocyte long chain fatty acid uptake in Osborne–Mendel and S5B/Pl rats in response to high-fat diets

To determine whether strain differences in adipocyte uptake of long chain fatty acids (LCFAs) contribute to differences in weight gain by Osborne-Mendel (OM) and S5B/Pl rats (S) fed a high-fat diet (HFD). Ninety-four adult (12-14-week old) male OM and S rats. Body weight; epididymal fat pad weight; adipocyte size, number, LCFA uptake kinetics; and plasma insulin and leptin during administration of HFD or chow diets (CDs). In both strains, rate of weight gain (RWG) was greater on an HFD than a CD; RWG on an HFD was greater, overall, in OM than S. A significant RWG increase occurred on days 1 and 2 in both strains. It was normalized in S by days 6-9 but persisted at least till day 14 in OM. RWGs were significantly correlated (P<0.001) with the V(max) for saturable adipocyte LCFA uptake (V(max)). In S, an increase in V(max) on day 1 returned to baseline by day 7 and was correlated with both plasma insulin and leptin levels throughout. In OM, a greater increase in V(max) was evident by day 2, and persisted for at least 14 days, during which both insulin and leptin levels remained elevated. Growth in epididymal fat pads on the HFD correlated with body weight, reflecting hypertrophy in OM and both hypertrophy and hyperplasia in S. (a) Changes in V(max) contribute significantly to changes in RWG on HFDs. (b) There are important strain differences in circulating insulin and leptin responses to an HFD. (c) Both insulin and leptin responses to an HFD are closely correlated with V(max) of adipocyte fatty acid uptake in S animals, but suggest early onset of insulin resistance in OM. Thus, differences in hormonal regulation of adipocyte LCFA uptake may underlie the different responses of OM and S to HFD.

An Albumin-Exendin-4 Conjugate Engages Central and Peripheral Circuits Regulating Murine Energy and Glucose Homeostasis

Glucagon-like peptide-1 (GLP-1) regulates glucose homeostasis through multiple mechanisms including direct actions on the endocrine pancreas and indirect activation of central nervous system circuits regulating gastric emptying, satiety, and body weight. Because native GLP-1 is rapidly degraded, there is considerable interest in development of more potent GLP-1 receptor (GLP-1R) agonists with sustained activity; however, the extent to which much larger GLP-1R agonists will mimic some or all of the actions of smaller peptides remains uncertain. We studied the actions of CJC-1134-PC, a recombinant human serum albumin-exendin-4 conjugated protein, at the GLP-1R using heterologous cells expressing the GLP-1R in vitro and both wild-type and Glp1r(-/-) mice in vivo. CJC-1134-PC activated GLP-1R-dependent signaling in baby hamster kidney-GLP-1R cells and acutely lowered blood glucose in wild-type but not in Glp1r(-/-) mice. Moreover, acute administration of CJC-1134-PC rapidly activated c-Fos expression in multiple regions of the central nervous system, acutely inhibited gastric emptying, and produced sustained inhibition of food intake in a GLP-1R-dependent manner. Furthermore, chronic daily treatment of high-fat diet-fed wild-type mice with CJC-1134-PC for 4 weeks led to improved glucose tolerance, increased levels of glucose-stimulated insulin, decreased HbA1c, and weight loss associated with decreased hepatic triglyceride content. These findings illustrate that a high-molecular-weight exendin-4-albumin conjugate retains the ability to mimic a full spectrum of GLP-1R-dependent actions, including activation of central nervous system circuits regulating gastric emptying, food intake, and body weight.

Group IVA phospholipase A 2 is associated with the storage of lipids in adipose tissue and liver

Prostaglandin (PG) E 2 is considered to participate in the storage of fat in adipocytes and hepatocytes, but roles of group IVA phospholipase A 2 (PLA 2), a key PLA 2 isozyme in the arachidonic acid cascade, remain unclear. The present study examined the possible involvement of the enzyme using group IVA PLA 2-deficient mice (C57BL/6 background, 22 weeks of age) fed a normal diet (5.3% fat). The ratio of epididymal fat pad weight to body weight was significantly reduced in group IVA PLA 2-deficient mice compared to wild-type mice. Histological analysis revealed that in group IVA PLA 2-deficient mice, the adipocytes were smaller, and hepatocytes bearing cytoplasmic vacuolation were scarce. Hepatic triglyceride content and the serum levels of PGE 2 in the deficient mice were also lower. However, there was no difference in the serum levels of insulin, glucose, non-esterified free fatty acid, or total cholesterol between the deficient and wild-type mice. Our findings suggest that group IVA PLA 2 is involved in the storage of lipids in the adipose tissue and liver and in determining circulating PGE 2 levels.

Anti-Obesity and Hypolipidemic Effects of Black Soybean Anthocyanins

The effect of anthocyanins extracted from black soybean (Glycine max L.) seed coats on body weight, adipose tissue weight, and serum lipids was evaluated in rats fed a high fat diet (HFD). Rats were raised on a normal diet (ND) (based on the AIN-93M diet), HFD (ND supplemented with 16% lard oil), HFD containing 10% black soybean, and HFD containing 0.037% black soybean anthocyanins (equivalent to that in the 10% black soybean diet). Weight gain was significantly lowered in the rats fed HFD plus black soybean anthocyanins compared with the rats fed HFD alone (P < .05) and reversed to the level of the rats fed ND. The black soybean diet also decreased body weight gain compared with the HFD (P < .05). The black soybean anthocyanins-added diet suppressed the HFD-induced weight gain in liver intermediately and tended to decrease the weights of epididymal and perirenal fat pads. The black soybean anthocyanins were also effective in improving the lipid profile. They significantly reduced the levels of serum triglyceride and cholesterol (P < .05), while they markedly increased the high-density lipoprotein-cholesterol concentration, which was decreased in the rats fed HFD (P < .05). These results indicate that the anthocyanins in black soybean seed coats have an anti-obesity effect, which can reverse the effects of HFD on body weight, adipose tissue weight, and serum lipid contents.

Dietary chickpeas reverse visceral adiposity, dyslipidaemia and insulin resistance in rats induced by a chronic high-fat diet

The improved effects of dietary chickpeas on visceral adiposity, dyslipidaemia and insulin resistance were examined. Rats were fed a normal-fat diet (NFD), a high-fat diet (HFD) or a high-fat plus chickpea diet (HFD+CP) for 8 months. The epididymal fat pad weight v. total body weight of rats was higher in the HFD group (0.032 (sd 0.0042) g/g) than in the NFD group (0.015 (sd 0.0064) g/g) and smaller in the HFD+CP group (0.023 (sd 0.0072) g/g) compared with the HFD group (P < 0.05). Chickpea treatment also induced a favourable plasma lipid profile reflecting decreased TAG, LDL-cholesterol (LDL-C) and LDL-C:HDL-cholesterol levels (P < 0.05). HFD-fed rats had higher TAG concentration in muscle and liver, whereas the addition of chickpeas to the HFD drastically lowered TAG concentration (muscle, 39 %; liver, 23 %). The activities of lipoprotein lipase (LPL) in epididymal adipose tissue and hepatic TAG lipase in liver recorded a 40 and 23 % increase respectively in HFD rats compared with those in NFD rats; dietary chickpeas completely normalised the levels. Furthermore, chickpea-treated obese rats also showed a markedly lower leptin and LPL mRNA content in epididymal adipose tissue. An insulin tolerance test, oral glucose tolerance test and insulin-releasing test showed that chickpeas significantly improved insulin resistance, and prevented postprandial hyperglycaemia and hyperinsulinaemia induced by the chronic HFD. The present findings provide a rational basis for the consumption of chickpeas as a functional food ingredient, which may be beneficial for correcting dyslipidaemia and preventing diabetes.

Macrophage TNF-α contributes to insulin resistance and hepatic steatosis in diet-induced obesity

Obesity is commonly associated with development of insulin resistance and systemic evidence of inflammation. Macrophages contribute to inflammatory amplification in obesity and may contribute directly to insulin resistance and the development of nonalcoholic fatty liver disease through the production of inflammatory cytokines, including tumor necrosis factor (TNF)-alpha. To test this hypothesis, we transplanted male wild-type (WT) and TNF-alpha deficient (KO) mice with either TNF-alpha-sufficient (TNF-alpha(+/+)) or TNF-alpha-deficient (TNF-alpha(-/-)) bone marrow. After consuming a high-fat diet for 26 wk, metabolic and morphometric characteristics of the animals were analyzed. While there were no differences in terms of relative weight gain, body composition analysis yielded a lower relative adipose and higher relative lean mass in mice lacking TNF-alpha, which was partially explained by reduced epididymal fat pad and liver weight. TNF-alpha(-/-) -->KO mice exhibited enhanced insulin sensitivity compared with that observed in TNF-alpha(+/+)-->KO mice; remarkably, no protection against insulin resistance was provided by transplanting TNF-alpha(-/-) bone marrow in WT mice compared with TNF-alpha(+/+)-->WT. The preserved insulin sensitivity seen in TNF-alpha(-/-)-->KO mice provided protection against the development of hepatic steatosis. Taken together, these data indicate that macrophage-derived TNF-alpha contributes to the pattern and extent of fat accumulation and insulin resistance in diet-induced obesity; however, this contribution is negligible in the presence of host-derived TNF-alpha.

N‐butyldeoxynojirimycin causes weight loss as a result of appetite suppression in lean and obese mice

To determine the mechanism of weight loss caused by high doses of N-butyldeoxynojirimycin (NB-DNJ) in healthy lean and leptin-deficient obese (ob/ob) mice. Healthy lean and obese mice were treated with NB-DNJ by the following methods: admixed with their diet, delivered by subcutaneously implanted mini-pumps or by intraperitoneal or intracerebroventricular (ICV) injection. Daily changes in body weight and food intake were recorded during the experimental period. The effect of NB-DNJ treatment on subcutaneous adipose tissue and on epididymal fat pads was measured. Lean mice treated with NB-DNJ, admixed with their diet, lost weight in the form of adipose tissue. This resulted in a 40% reduction in skin thickness (control, 358 +/- 11 microm; NB-DNJ treated 203 +/- 6 microm) and a reduction in epididymal fat pad weights after 5 weeks of treatment at 2400 mg/kg/day (control, 0.0154 +/- 0.001; NB-DNJ treated, 0.0026 +/- 0.0005 as ratios of fat pad weight to total body weight). Following the depletion of adipose tissue mass, the mice grew normally and did not have any reduction in lean mass. Obese mice treated with NB-DNJ also lost weight or gained weight at a greatly reduced rate compared with non-treated controls. Body weights at 6 months of age were: lean control, 29.10 +/- 1.15 g; lean NB-DNJ treated, 22.73 +/- 0.29 g; obese control, 63.25 +/- 1.5 g; obese NB-DNJ treated from 5 weeks of age, 35.30 +/- 1.68 g; obese NB-DNJ treated from 12 weeks of age, 38.84 +/- 1.26 g. Both the lean and obese groups of mice treated with NB-DNJ ate up to 30% less than untreated controls. Daily food intake (powder diet) were: lean control, 4.15 +/- 0.54 g; obese control, 4.14 +/- 0.2 g; lean NB-DNJ treated 2.9 +/- 0.37 g; obese NB-DNJ treated, 2.88 +/- 0.47 g. Mice treated with the N-substituted galactose imino sugar analogue, N-butyldeoxygalactonojirimycin (NB-DGJ) did not lose weight. Mice experienced similar weight loss or lack of weight gain when fed a restricted diet that mimics the drug-induced level of food consumption. Delivery of 2 nmol NB-DNJ by ICV injection into lean mice also caused similar reductions in food intake. Food intake: saline vehicle, 4.30 +/- 0.12 g; NB-DNJ, 3.37 +/- 0.19 g; NB-DGJ, 4.03 +/- 0.16 g; 2-deoxyglucose, 4.7 +/- 0.15 g. NB-DNJ causes weight loss as a result of reduced food consumption due to central appetite suppression.

Effect of maternal vitamin and mineral restrictions on the body fat content and adipocytokine levels of WNIN rat offspring

BackgroundIntrauterine growth retardation due to maternal under-nutrition increases susceptibility to obesity and insulin resistance. We reported earlier in the offspring of mineral or vitamin restricted rat dams, a high body fat percentage and decreased insulin secretion to glucose challenge. This study determined whether or not central adiposity and altered adipocytokine profile were associated with high body fat content.MethodsBody fat percentage; glucose, insulin and adipocytokine levels in fasting plasma and fresh weights of epididymal fat pads were determined in the six months old male offspring of Wistar NIN rat dams on chronic 50 percent restriction of vitamins or minerals throughout their growth, gestation, lactation and weaned on to restricted diets or restricted mothers/offspring rehabilitated from different time points.ResultsIn line with high body fat percent, chronic restriction of vitamins and minerals increased the epididymal fat pad weight. Maternal vitamin restriction decreased plasma adiponectin and increased leptin levels whereas mineral restriction decreased both. Both the treatments did not affect plasma TNF-α levels or insulin resistance status (HOMA-IR). Rehabilitation from parturition but not weaning, rescued the changes in the offspring.ConclusionHigh body fat percentage in the offspring of vitamin restricted or mineral restricted rat dams was associated with increased abdominal adiposity (epididymal fat pad weight) and differential expression of adipocytokines but not insulin resistance. The changes could be mitigated by rehabilitation from birth but not weaning.

Kakkalide and Irisolidone: HMG-CoA Reductase Inhibitors Isolated from the Flower of Pueraria thunbergiana

As part of our search for anti-arteriosclerosis agents from traditional Chinese medicines, the 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HCR)-inhibitory constituent, kakkalide, was isolated from the flower of Pueraria thunbergiana (PT, family Leguminosae). The antihyperlipidemic effects of kakkalide and its metabolite, irisolidone, which may be a bioactive form in vivo and potently inhibit the HCR activity, were investigated in vivo. Both the oral and interperitoneal administrations of kakkalide and irisolidone, with the exception of intraperitoneally treated kakkalide, potently lowered the serum levels of total cholesterol (TC) and triglyceride (TG) in Trition WR1339-induced hyperlipidemic mice. The oral administrations of kakkalide and irisolidone in hyperlipidemic mice induced, by the long-term feeding of a high fat diet, also potently reduced the serum levels of TC and TG and epididymal fat pad weight. These findings suggest that PT can improve hyperlipidemia, and the hypolipidemic effect may be due to HMG-CoA reductase.

콜레스테롤 식이를 섭취한 흰쥐에 새송이버섯이 지질대사 및 효소활성에 미치는 영향

새송이버섯이 고콜레스테롤 식이를 섭취한 흰쥐의 지질대사에 미치는 영향을 조사하고자, 생후 8주령 숫쥐를 정상식이군, 대조식이군(5% 옥수수기름, 5% 돈지 및 0.5% 콜레스테롤을 첨가한 식이) 및 대조식이에 새송이버섯 분말을 3% 및 5%씩 첨가한 식이군 (3% 및 5% 새송이버섯군) 등 4군으로 나누어 4주간 사육한 결과는 다음과 같다. 실험동물의 체중증가량 및 식이효율은 대조군에 비하여 3% 및 5% 새송이버섯군이 유의하게 감소되었다. 간과 부고환지방의 무게는 대조군에 비해 5% 새송이버섯군이 유의하게 감소되었다. 간의 콜레스테롤 및 중성지질 농도는 대조군에 비하여 5% 새송이버섯군이 유의하게 감소되었다. 혈청의 중성지 질, 총 콜레스테롤과 LDL+VLDL-콜레스테롤 농도 및 동맥경화지수는 대조군에 비해 새송이버섯군들이 유의하게 감소되었다. 총 콜레스테롤에 대한 HDL-콜레스테롤의 비율은 대조군에 비해 새송이버섯군들이 유의하게 증가되었다. 변의 지질배설량은 5% 새송이버섯군이 대조군 보다 유의하게 증가된 것으로 나타났다 이상의 결과로 보아 고콜레스테롤 식이에 새송이버섯 분말 첨가 급여시 흰쥐의 일부 지질대사를 개선시키는 것으로 나타났다. Effects of dietary supplementation of Pleurotus eryngii(PE) to a diet containig the cholesterol on lipid levels in the liver and serum, and enzyme activities of rats were studied by feeding 8-weeks old male rats with the four diets for 4 weeks, respectively: normal diet, control diet (10% fat + 0.5% cholesterol), 3% and 5% PE diets (control diet + 3% and 5% PE dry powder). The body weight gains and food efficiency ratios of the 3% and 5% PE diet groups were significantly lower than those of the control group. The liver and epididymal fat pad weights, and hepatic triglyceride Levels of the 5% PE diet group were more significantly decreased than those of the control group. The concentrations in serum triglyceride, total cholesterol, LDL+VLDL-cholesterol, and atherogenic index ratios were significantly lower in the 3% or 5% PE groups compared to those of the control group. Ratio of HDL-cholesterol to total-cholesterol was significantly higher in the 3% and 5% PE groups compared to that of the control group. The fecal total lipid excretion of the 5% PE diet group was more significantly decreased than that of the control group. There was no significant difference in the hepatic cholesterol, and the serum HDL-cholesterol concentrations, and the GOT, GPT and <TEX>${\gamma}-GTP$</TEX> activities among the experimental groups. These results showed that the Pleurotus eryngii powder feeding decreased the total cholesterol, LDL-cholesterol and atherogenic index, and increased the ratio of HDL-cholesterol to total-cholesterol in serum of the rats.

Inactivity induces increases in abdominal fat

Previously, inducing inactivity for 53 h after 21 days of voluntary running resulted in a 25 and 48% increase in epididymal and omental fat pad weights, respectively, while rats continued to eat more than a group that never had access to a running wheel (J Physiol 565: 911-925, 2005). We wanted to test the hypothesis that inactivity, independent of excessive caloric intake, could induce an increase in fat pad mass. Twenty-one-day-old rats were given access to voluntary running wheels for 42-43 days so that they were running approximately 9 km/day in the last week of running, after which wheels were locked for 5, 53, or 173 h (WL5, WL53, WL173) before the rats were killed. During the 53 and 173 h of inactivity, one group of animals was pair fed (PF) to match sedentary controls, whereas the other continued to eat ad libitum (AL). Epididymal and retroperitoneal fat masses were significantly increased in the WL173-PF vs. the WL5 group, whereas epididymal, perirenal, and retroperitoneal fat masses were all significantly increased in the WL173-AL group compared with the WL5 group. Additionally, hyperplasia, and not hypertrophy, of the epididymal fat mass was responsible for the increase at WL173-AL as demonstrated by a significant increase in cell number vs. WL5, with no change in cell diameter or volume. Thus two important findings have been elucidated: 1) increases in measured abdominal fat masses occur in both AL and PF groups at WL173, and 2) adipocyte expansion via hyperplasia occurred with an ad libitum diet following cessation of voluntary running.

NEW INVESTIGATOR AWARD FINALISTS NIA0001 Induction of differentiation in human preadipocytes may contribute to adipogenic effect of human adenovirus Ad‐36

Human adenovirus Ad‐36 causes adiposity in animal models and shows association with human obesity. The mechanism involved is unknown. We previously reported that Ad‐36 enhances differentiation of 3T3‐L1 preadipocytes and E4orf‐1 gene of the virus is responsible for the adipogenic effect in the rodent cell line. We undertook a three‐step approach to investigate the role of preadipocyte differentiation in adipogenic effect of Ad‐36. First, we showed that the viral mRNA is expressed in adipose‐derived stem cells (ASC) of animals experimentally infected with Ad‐36. Infection of rats with Ad‐36 resulted in increased epididymal fat pad weight and the expression of Ad‐36 E4orf‐1 mRNA was detected in ASC isolated from the fat pads. Next, we determined if humans naturally infected with Ad‐36 will show greater preadipocyte differentiation. Subcutaneous adipose‐tissue samples from 33 Pima Indian subjects were screened by nested‐PCR specific for Ad‐36 DNA. Nine subjects (27%) had Ad‐36 DNA. A blinded comparison of their ASC showed greater differentiation to adipocytes for the Ad‐36 DNA positive subjects (P = 0.06) compared to the Ad‐36 DNA negative group. Finally, we used a direct approach. Human‐ASC when infected with Ad‐36 showed spontaneous replication, differentiation, and lipid accumulation, which was significantly greater than the uninfected controls (P &lt; 0.01). Ad‐36 induced lipid accumulation in human‐ASC increased in response to the viral load and the lipogenic response was observed regardless of the donor gender and over an age range of 22–57 years. These results suggest that ability of Ad‐36 to induce preadipocyte differentiation may play a role in human adiposity.

Desaturation indices in liver, muscle, and bone of growing male and female mice fed trans‐10, cis‐12 conjugated linoleic acid

trans-10,cis-12-CLA (t10,c12-CLA) inhibits lipid deposition in adipose tissue of many species, but it also enhances lipid deposition in liver. We evaluated effects of dietary t10,c12-CLA content and gender on carcass composition, FA profile of selected tissues, and expression of FA synthase (FAS) and stearoyl-CoA desaturase-1 (SCD) mRNA in adipose tissue. Male and female (63 of each) CD-1 mice were assigned a diet containing 0.0, 0.15, or 0.30% t10,c12-CLA at 4 wk of age. Seven mice per dietary group within gender were sacrificed after 2, 4, or 6 wk. The CLA isomer caused dose-dependent reductions in dry carcass weight and fat content, without altering protein content, but carcass fat and epididymal fat pad weights of males were reduced to a greater extent than carcass fat and inguinal fat pad weights of females. FAS and SCD mRNA in adipose tissue was more abundant in females than males, but expression in both genders decreased as the t10,c12-CLA content of the diet increased. Although the weight of gastrocnemius muscle was not influenced by diet, total FA content of the muscle of both genders decreased in response to dietary t10,c12-CLA content. Femur weight of male mice increased as the t10,c12-CLA content of the diet increased, but the weight increase was associated with a reduction in total FA content. The delta 9 desaturation indices for muscle and femur suggested a linear reduction in SCD activity, whereas delta 9 indices for liver indicated linear enhancement of SCD activity. Overall, results suggested that growing male mice were more susceptible than females to t10,c12-CLA inhibition of lipid deposition.