Fat Cell Diameter Research Articles

Young sheep of Romanov breed: productivity and biological features at different levels of energy and protein in the diet

The experiment was performed on two groups of Romanov sheep at the age of from 3 to 10 months under different rearing and fattening conditions at the “Pokrov” sheep farm in the Tver region. An increase in metabolic energy and crude protein in the diets of animals from 3 to 7 months of age led to an increase in the growth intensity of the body weight in Group II. The live weight of rams at the age of 7 months was greater by 5.79 kg or 17.75% in Group II than in Group I, and the daily gain increased from 138 g to 186 g. In terms of the daily gain, the difference at this age was 45 g or 32.37%. According to the slaughter results, the pre-slaughter weight of the rams in Group II increased by 9.73 kg or 22.3% compared to Group I; the hot carcass weight was greater by 5.08 kg or 25.5%; the slaughter weight by 6.4 kg or 31.1 %; and the slaughter yield increased from 47.3% to 50.7%, or by 3.4 absolute percent. The histological studies of the longissimus muscle showed, that in Group II, the diameter of muscle fibers increased by 4.3 μm or 15.7%, the diameter of fat cells by 6.2 μm or 10.4%; and the numbers of muscle and fat cells per 1 cm2 of the longissimus muscle increased and amounted to 5.6 and 28.6%, respectively. The width of the connective tissue decreased by 5.2 μm or 14.7%. The difference in the amounts of wool shorn—original and clean fiber—was 0.27 and 0.20 kg or 20.1 and 21.1% in favor of Group II animals with an increased level of energy and protein in their diets. The histological studies of skin showed, that the total skin of rams in Group II (at intensive feeding) was thicker by 523 μm or 22.6% than in Group I, with the pilar layer being thicker by 231 μm or 15.1%. The thickness of the reticular layer increased by 290.5 μm or 38.8% in young animals of Group II. The 3-7 month old Romanov rams with the live weight of 16-38 kg and 186 g of the daily body weight gain had requirements for 1.45 kg of dry matter (DM), 1.50 energetic feed units (EFU) of exchange energy, and 186 g of crude protein per 1 head a day at a cost of 7.8 kg of DM, 8.06 EFU of metabolic energy, and 988 g of crude protein per 1 kg of increase.

Effect of Forskolin on Body Weight, Glucose Metabolism and Adipocyte Size of Diet-Induced Obesity in Mice.

Simple SummaryObesity has become a global pandemic involving an increase in the amount and size of fat cells in the body. Obesity is highly associated with insulin resistance and type 2 diabetes. Several medicinal plants have been reported to be useful in the prevention of obesity. Forskolin, a bioactive compound of Coleus forskohlii, can promote lipolysis in mature adipocytes. However, the effect of forskolin on body weight, glucose metabolism and adipocyte size of diet-induced obesity is still rarely investigated. In this study, the effects of forskolin on the high-fat diet-induced obese model were evaluated. Results showed that forskolin administration improves glucose metabolism and reduces fat cell diameter in the high-fat diet-fed mice. Forskolin also suppresses adipocyte differentiation of murine mesenchymal stem cells.The purpose of this study was to investigate the effects of forskolin on body weight, glucose metabolism and fat cell diameter in high-fat diet-induced obese mice. Four-week-old male mice (C57BL/6) were randomly assigned to 1 of 3 treatment groups: a high-fat diet plus 5% dimethyl sulfoxide (vehicle), high-fat diet plus 2 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide) and high-fat diet plus 4 mg/kg of forskolin (dissolved in 5% dimethyl sulfoxide). Forskolin or dimethyl sulfoxide was administered intraperitoneally every two days. The results indicated that no significant difference was observed in the body weight, feed intake and serum lipid parameters among groups at 20 weeks of age. The blood glucose levels were significantly reduced in the groups treated with 2 mg/kg of forskolin before glucose tolerance test. Forskolin administration linearly decreased blood glucose levels of high-fat diet-fed mice at 90 min and total area under curve (AUC) after insulin tolerance test. The subcutaneous adipocyte diameter was significantly reduced in the groups treated with 2 mg/kg of forskolin. Forskolin administration linearly reduced the gonadal adipocyte diameter of high-fat diet-fed mice. Forskolin significantly reduced the differentiation of murine mesenchymal stem cells into adipocytes and this was accompanied by a decrease in intracellular triglyceride content and an increase in glycerol concentration in the culture medium. The subcutaneous adipocyte diameter, gonadal adipocyte diameter and total AUC of insulin tolerance test were moderately negatively correlated with the concentration of forskolin in the high-fat diet-induced obese model. These results demonstrate that forskolin can regulate glucose metabolism and reduce fat cell diameter of high-fat diet-fed mice and inhibit the adipocyte differentiation of murine mesenchymal stem cells.

Carya cathayensis leaf extract attenuates ectopic fat deposition in liver, abdomen and aortic arch in ovariectomized rats fed a high-fat diet

BackgroundCarya cathayensis1is a commercially cultivated plant in the Zhejiang Province, China. Its nuts exhibit properties of tonifying kidneys and relieving asthma. There have been a few pharmacological studies addressing the function of the leaves of this plant. Our previous studies on C. cathayensis leaf extract (CCE) showed a significant inhibitory effect on weight gain in mice fed a high-fat diet, particularly in female mice. Hypothesis/purposeTo investigate the biological and molecular mechanisms underlying the regulation of ectopic adipose tissue deposition by CCE in ovariectomized rats fed a high-fat diet. Study designFemale Sprague–Dawley rats were ovariectomized and treated with CCE (50, 100, and 200 mg/kg body weight, oral) or estradiol (1 mg/kg body weight, oral) for 8 weeks. MethodsCCE was subjected to high-performance liquid chromatography to quantify major components. Body weight gain, abdominal fat coefficient, and aortic arch fat coefficient were determined; serum was collected for biochemical analysis; tissues were collected for histopathological examination, quantitative polymerase chain reaction (Q-PCR), and western blotting. ResultsThe total flavonoid content was determined to be 57.30% in the CCE and comprised chrysin, cardamomin, pinostrobin chalcone, and pinocembrin. Compared with the model group (OVX), CCE treatment reduced body weight gain, abdominal and aortic arch fat coefficients, serum and hepatic lipid profiles, including total cholesterol (TC), total triglycerides (TG), and free fatty acids (FFA) levels; decreased lipid droplets in liver cells; decreased fat accumulation in the aortic arch blood vessel wall and increased its smoothness; decreased the diameter of abdominal fat cells; and reduced serum leptin and adiponectin levels significantly. Serum adiponectin levels significantly correlated with serum TG and hepatic TC levels. Leptin levels positively correlated with serum TG levels and negatively correlated with hepatic TG. Leptin mRNA, peroxisome proliferator-activated receptor (PPARγ) mRNA, and protein expression levels in abdominal adipose tissue were significantly down-regulated. Adiponectin mRNA levels were slightly reduced but not significantly. ConclusionCCE attenuated ectopic fat deposition induced by deficient estrogen and a high-fat diet in rats; this may be associated with activated leptin sensitivity, improved leptin resistance, and regulated adiponectin levels. CCE may improve adipose function to regulate adipocyte differentiation by down-regulating PPARγ. Overall, these results suggest that CCE is a potential phytoestrogen.

Growth, behavioural, serum biochemical and morphological changes in female rabbits fed high-fat diet.

This study aimed to determine whether high-fat diet (HFD) could cause growth, behavioural, biochemical and morphological changes in young female rabbits. Thirty-six female rabbits were randomly divided into two groups fed with either a high-fat diet (HFD) or a standard normal diet (SND) for 5weeks. Growth and behavioural changes were recorded during the 5-week feeding period. Tissue samples, including blood and adipose tissue, were obtained after slaughter. HFD rabbits weighed more by the end of the feeding period, had a higher percent body weight and adipose tissue weight change and had longer body and bust lengths than SND rabbits. HFD rabbits significantly reduced their feed intake and feeding frequency during the fourth and fifth weeks. HFD rabbits also showed lower frequency of drinking and resting and increased stereotypical behaviour. Besides, HFD rabbits showed significant physiological abnormalities. HFD rabbits had higher serum cholesterol (TC) and triglycerides (TG) levels than SND rabbits at the end of the feeding period, and higher free fatty acid (FFA) levels than rabbits in the SND group after the third week of feeding. Serum thyroxine (T4) increased significantly in week 2 and week 5 and triiodothyronine (T3) increased significantly in week four. However, there was no significant change in serum glucose (GLU) and insulin (INS) levels. Additionally, HFD reduced the area and diameter of perirenal and subcutaneous fat cells and increased their density. Our findings suggest that HFD rabbits had higher weight gains, accumulation of fat, and more behavioural changes than SND rabbits. Although high levels of fat in the diet had a low impact on hyperglycaemia, it could lead to hyperlipidemia and hyperthyroidism. Our results also suggest that sustained HFD may cause the proliferation of adipocytes in young female rabbits.

Expression of Sirtuin 1 in visceral adipose tissue in Tibetan mini-pigs with obesity and insulin resistance induced by high fat/cholesterol diet

To investigate the role of Sirt1 in visceral adipose tissue in Tibetan mini-pigs with obesity and insulin resistance induced by high fat/cholesterol diet. Twelve male Tibetan mini-pigs were divided into 2 groups randomly: normal control (NC) group, high-fat/cholesterol (HFC) diet group, 6 in each group. After 16 weeks of modeling, fasting body weight and body mass index (BMI) were measured. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were measured in anterior venous blood, and atherosclerosis index (AI) was calculated. Meanwhile, intravenous glucose tolerance test was conducted to observe the changes of blood glucose and insulin, and the area under the curve (AUC) was calculated. After euthanasia, visceral fat rate was detected, and visceral fat tissue was taken for histopathological observation and fat cell diameter analysis. RT-PCR was used to observe the mRNA expression levels of Sirtuin1 (Sirt1), insulin-like growth factor-1 (IGF-1), glucose transporter 4 (GLUT4), peroxisome proliferator-activated receptor γ (PPARγ), peroxisome proliferator-activated receptor γ-assisted activator 1α (PGC-1α), forkhead box protein O1 (FoxO1), lipolysis-related gene hormone-sensitive lipase (HSL), and fat synthesis-related gene fatty acid synthase (FASN)changes in adipose tissue. Compared with the NC group, the body weight, BMI, TC, LDL-C, HDL-C, AI and visceral fat rate were significantly increased after 16 weeks of high-fat/cholesterol induction in Tibetan mini-pigs(P＜0.05,P＜0.01). Meanwhile, the glucose tolerance curve was significantly delayed and the area under the curve of blood glucose and insulin was significantly increased (P＜0.05). HE pathological observation and quantitative analysis showed that fat cells were hypertrophy and the average cell diameter was increased significantly (P＜0.01). In addition, the mRNA expression levels of Sirt1,PGC-1α, GLUT4, and HSL were all decreased in varying degrees in adipose tissue, among which the mRNA expressions of Sirt1 and HSL were significantly decreased (P＜0.05), while the mRNA expressions of FOXO1, IGF-1, PPARγ, and FASN were significantly increased (P＜0.05, P＜0.01). Tibetan mini-pigs were induced by high fat/cholesterol diet to form obesity model with phenotypic characteristics such as lipid disorder and insulin resistance, whereas Sirt1 plays a key role in visceral fat deposition and insulin sensitivity reduction in obese Tibetan mini-pigs.

Effects of dihydromyricetin on high fat diet induced obesity in mice and its mechanism

To observe the effects of dihydromyricetin (DHM) on obesity induced by high-fat diet in mice, and to explore whether its mechanism of action is related to the promotion of WAT browning. Sixty c57bl/6j mice were randomly divided into 6 groups (n=10): ①normal control group (ND group): normal feed feeding; ②Normal control + low dose DHM group (ND+L-DHM group): normal feed feeding was treated with low dose DHM (125 mg/(kg·d)); ③Normal control + high dose DHM group (ND+H-DHM group): normal feed feeding was treated with high dose DHM (250 mg/(kg·d)); ④High-fat diet group (HFD): high-fat diet; ⑤high-fat diet + low-dose DHM group (HFD+L-DHM group): high-fat diet feeding with low-dose DHM; ⑥High-fat diet + high-dose DHM group (HFD+H-DHM group): High-fat diet was treated with high-dose DHM. After 16 weeks, the mice were fasted overnight, blood samples were collected for fasting blood glucose and blood lipids, then the animals were sacrificed, body length was measured, and Lee's index was calculated. After weighing the adipose tissue in the scapula, groin and epididymis, formaldehyde fixation and HE staining were used to observe the fat cells size, immunohistochemistry was used to detect the expression of uncoupling protein 1 (UCP1). The body weight was measured every 4 weeks during the experiment. Compared with the ND group, the body weight of the mice in the HFD group was increased significantly, suggesting that the obese mouse model replicated successfully. In addition, the body fat weight, fat cell diameter, Lee's index and blood glucose of the HFD group were increased significantly, and the expression of UCP1 in the adipocytes was increased. Body weight, fat cell diameter, Lee's index and blood glucose of HFD mice treated with L-DHM and H-DHM were reversed significantly, while the expression of UCP1 in adipocytes was more significantly increased; however, L-DHM and H-DHM had no significant effects on the above indicators in normal mice. Dihydromyricetin inhibited high fat diet induced mouse obesity; the mechanism might be associated with promoting WAT browning.

The cell cycle pathway regulates chicken abdominal fat deposition as revealed by transcriptome sequencing

With the improvement of growth traits and feed conversion rate, the abdominal fat rate of Chinese local breeds of broilers has been increasing. Excessive abdominal fat deposition not only reduces the slaughter rate and disease resistance of broiler chickens, but also produces waste due to the difficulty of fat treatment. In order to study the regulatory genes and pathways involved in abdominal fat deposition of broilers, we used high-fat diets to feed the Xinghua Chicken, which is a Chinese local breed. Two weeks after feeding, we found that the abdominal fat weight and rate of broilers in the high-fat diet group increased significantly, and the diameter and area of abdominal fat cells also increased significantly. Transcriptome sequencing of abdominal fat and livers showed that the differentially expressed genes in the abdominal fat were mainly enriched in the cell cycle, peroxisome proliferator- activated receptor (PPAR) and extracellular matrix (ECM) receptor signaling pathways. The differentially expressed genes in livers were also significantly enriched in the cell cycle pathway, as well as in the steroid biosynthesis and PPAR signaling pathway. By analyzing the common differentially expressed genes in abdominal fat and liver tissues, we found that these genes were also enriched in cell cycle. Finally, we used the chicken LMH (chicken hepatoma cell) cell line and chicken ICP (immortalized chicken preadipocytes) cell line to do the in vitro validation assays. We used high-fat and common medium to culture the cells. The results showed that after 48 hours, the high-fat medium could significantly promote cell cycle and increase the number of cells in S phase. Additionally, qRT-PCR results showed that the high-fat medium could significantly promote the expression of genes related to cell cycle. In conclusion, we found that high-fat diets activate the cell cycle progression of chicken hepatocytes and preadipocytes, promote cell proliferation, and then increase abdominal fat deposition.

Peran kecambah kacang hijau (Phaseolus radiatus (L.)) pada sel lemak retroperitoneal tikus Sprague Dawley yang diberi diet tinggi lemak

The role of mung bean sprouts (Phaseolus radiatus (L.)) on retroperitoneal fat cells of Sprague Dawley rats fed a high-fat dietBackground: The tendency of current lifestyles with high consumption patterns of fat is one of the factors causing obesity which is a risk of cardiovascular disease. Prevention of cardiovascular disease can be done by adopting a dietary pattern that is rich in antioxidants including consumption of sources of vitamin E. Sprouts from mung beans contain vitamin E and phytochemicals rich in antioxidants, so they can be used as an alternative to prevent hyperlipidemia sourced from daily functional food.Objective: To assess the effects of mung bean sprouts on retroperitoneal fat weight, cell number and cell diameter in rats fed high-fat feed.Method: This research is an experimental study with a post-test design with the control group. Thirty-four male Sprague Dawley rats ± 2 months old were divided into five groups, group I (standard feed), group II (high-fat feed), group III (high-fat feed and intervention of feeding tube of mung bean sprout 0.67 g/ 200 g BW), group IV (high fat feed and intervention of feeding tube of mung bean sprout 1.34 g / 200 g BW), and group V (high-fat feed and 23 IU dose of vitamin E supplement with feeding tube). After adaptation for three days, the intervention was carried out for four weeks. Analysis of fat weight, fat cell number, and fat cell diameter were done after the treatments. Data analysis using the One-Way ANOVA test. Results: Mung bean sprout dose of 1.34 g given for 4 weeks did not significantly decrease fat weight and cell number, but it decreased the diameter of retroperitoneal fat cells.Conclusion: Mung bean sprouts dose 1.34 g was better than a dose of 0.67 g and vitamin E supplementation in reducing the diameter of retroperitoneal fat cells in rats fed a high-fat diet.

Electroacupuncture Reduces Body Fat by Down-regulating IL-6 and Vimentin in Abdominal White Adipose Tissue of Diet-induced Obesity Rats

To investigate the effect of electroacupuncture (EA) on IL-6 and vimentin protein expression in white adipose tissue (WAT) of diet-induced obesity (DIO) rats, so as to reveal its mechanism underlying losing weight. Thirty-four Wistar rats were randomly divided into normal (control, n＝10), model, sham-EA and EA groups (n＝8 in each of the latter 3 groups). The obesity model was established by feeding the rats with high fat diet. EA (2 Hz/15 Hz, 1 mA) was applied to bilate-ral "Zusanli "(ST 36) and "Tianshu "(ST 25) for 30 min, 5 times per week for a total of 8 weeks. For sham-EA group, two sham points (about 5 mm lateral to ST 36 and to ST 25) were only punctured with filiform needles but without electrical stimulation. Du-ring EA treatment, all rats were fed with normal fodder, and their body weight were measured once a week. Histopathologic changes (diameters of adipose cells) of abdominal WAT were observed under microscope after sectioning and H．E. staining, and the expression levels of IL-6 and vimentin in the WAT were detected by Western blot. Compared with the control group, the body weight, diameter of fat cells and the expression levels of IL-6 and vimentin in the WAT were significantly increased in the model group (P<0.05). Following EA, the body weight, diameter of fat cells and the expression levels of IL-6 and vimentin proteins were considerably down-regulated in the EA group (P<0.05), rather than in the sham-EA group relevant to the model group (P>0.05)．. EA intervention can effectively down-regulate the expression of IL-6 and vimentin in WAT of DIO rats, which may contribute to its action in reducing body fat by relieving chronic inflammation.

The difference in synovitis (synovial membrane) and angiogenesis between young obese, young lean and old lean people with primary knee osteoarthritis

Purpose: OA is a complex disorder with multiple risk factors including obesity. The excess weight and lipids inherent in obesity have been implicated in the development of OA through mechanical and metabolic effects and low-grade inflammation. Furthermore, synovitis and inflammation have gained an enhanced significance in research as a cause of OA. The aim of this laboratory research: 1: To determine the relationship between BMI and synovial vascularity and inflammation among different age groups with advanced OA. 2: To examine the effect of increased lipid stores as indicated by the fat cell size on the vascularity and inflammation. 3: To assess the difference in synovitis among young obese, young lean and old lean people with advanced OA. Methods: A total of 17 patients (matched for gender, the advanced stage of OA requiring total knee arthroplasty, Kellgren-Lawrence score, comorbidities, ASA grade, medications and functional outcome score) were recruited into three groups based on age (young <60, old >70) and BMI (lean <30, obese >30). Group-1: young-obese (N=6) with age and BMI mean (SD) 53.3 (2.33) and 38.53 (1.16) respectively. Group-2: young-lean (N=5) with age and BMI 55.60(4.5) and 27.01(1.59) respectively. Group-3: old-lean (N=6) with age and BMI 75.33 (3.2) and 25.64 (2.5) respectively. Synovial tissues obtained during surgery were examined using H&E staining and Immunohistochemistry (IHC) on 5μm sections. The monoclonal antibodies included vWF and CD34 for angiogenesis, CD68 for macrophage, CD3 for T-lymphocytes, CD20 for B-lymphocytes and vimentin for fibroblast (all Dako Ltd.). Visualization employed DAB. Quantitative assessment of each marker used image J software. Each slide was divided into synovial and fat sectors based on the content. The software measured each marker in the synovial and fat sectors separately and combined. Further analysis followed regrouping patients into two groups based on fat cell diameter, measured as small (< 68 μm) and large (>68 μm) fat cells. The IHC markers were reanalyzed based on the fat cell size. Additional manual counts, vessel diameter and distance to the synovial surface, were undertaken on vessels in the synovial and fat sectors. A synovitis score was determined using the H&E stained sections (Krenn et al., 2006). Results: Using the initial grouping, overall vascularity did not show any significant differences (p=0.468); vimentin positivity was significantly reduced in the old lean group (p=0.006), and inflammatory markers showed a trend of increasing with increase BMI. Regrouping patients based on fat cell size revealed multiple significant differences. Macrophages, T cells, B cells and fibroblasts positivity was significantly higher in the presence of big fat cells (p= 0.035, 0.016, 0.046, 0.014 respectively). The vascular density was significantly higher in the fatty sections with big fat cells (p= 0.028). Inflammatory markers showed positive correlation with BMI and negative correlation with age. An increasing trend of vascular density, the distance to the synovial surface and vascular wall thickness was observed in the young obese group. There was no clear difference between the groups in relation to synovitis but majority of patients showed mild grade synovitis. Conclusions: The synovium of the obese patients showed more inflammatory response but the vascularity was not significantly different. Increased fat cell size attracted significantly more inflammatory cells. Moreover, vascular hyperplasia, which was noticed mainly in the obese people, could be an indication of atherosclerosis in the synovial vessels. Low grade synovitis is common in primary knee OA. This image showed H&E stain of the synovium of an obese person. The vessels has increased wall thickness very close to the intimal surface.

Uncaria tomentosa (cat claw) Counteracts Chronic Fipronil-induced Endocrine Disruption Induced Insulin Resistance and Hepatic Damage in Male Albino Rats

The current study investigated the ability of Uncaria tomentosa (cat claw) to counteract fipronil (FIP) induced metabolic abnormalities. A total of 20 male adult albino rats were randomly divided into 4 groups (5 rats each). Control rats received only dis. water, Uncaria group was treated by dietary Uncaria 5g/kg, fipronil group rats treated with 3.23 mg/kg of FIP, and fipronil and Uncaria co-treated group was given 3.23 mg/kg FIP with 5g/kg dietary Uncaria. The doses were given every day for consecutive 12 weeks. Body weight, food intake and food conversion ratio (FCR) were determined. Blood samples were collected for estradiol and lipid profile estimation. Plasma liver enzymes were assayed. .Glucose and insulin were determined for Homa IR calculation. Liver tissues and abdominal fat were fixed for histopathological examinations. FIP-treated rats had no influence on body weight gain however, it increased (P<0.05) the food conversion ratio than other groups. Estradiol level was significantly (P<0.05) reduced by FIP however Uncaria ameliorated this decrease. Rats administrated FIP exhibited significantly higher cholesterol, triglycerides (TG), low-density lipoproteins (LDL) and liver enzymes (AST, and ALT) more than those in the other groups while it decreased (P<0.05) high-density lipoproteins (HDL). FIP produced a significant increase in insulin resistance (HOMA-IR) that was ameliorated by Uncaria. The liver of FIP-treated rats revealed vacuolar degeneration, lymphocytic infiltration and focal necrosis. Moreover, FIP increased diameter of fat cells. Uncaria combated FIP induced insulin resistance, liver damage and adiposity. Cat claw could effectively protect against metabolic disruption induced by FIP.

Expression of functional TSH receptor in white adipose tissues of hyt/hyt mice induces lipolysis in vivo

To determine the relative importance of TSH in white adipose tissue, we compared the adipose phenotypes of two distinct mouse models of hypothyroidism. These models differed in that the normal reciprocal relationship between thyroid hormone and TSH was intact in one and disrupted in the other. One model, thyroidectomized (THYx) mice, had a 100-fold increase in TSH and a normal TSH receptor (TSHR); in contrast, the other model, hyt/hyt mice, had a 120-fold elevation of TSH but a nonfunctional TSHR. Although both THYx and hyt/hyt mice were in a severe hypothyroid state, the epididymal fat (mg)/body wt (g) (F/B) ratio of THYx mice was much smaller than that of hyt/hyt mice (8.2 ± 0.43 vs. 14.4 ± 0.40, respectively, P < 0.001). The fat cell diameter in THYx mice was also smaller than that in hyt/hyt mice (79 ± 2.8 vs. 105 ± 2.2 μm, respectively, P < 0.001), suggesting that TSH induced lipolysis in adipose tissues. When we transferred a functional mouse TSHR gene and a control plasmid into opposite sides of epididymal fat of hyt/hyt mice by plasmid injection combined with electroporation, fat weight of the TSHR side was decreased to 60% of that of the control side. Messenger RNA levels of hormone-sensitive lipase in epididymal fat containing the transferred TSHR gene were twofold higher than those in tissue from the control side. These results indicated that TSH worked as a lipolytic factor in white adipose tissues, especially in mice in a hypothyroid state.

FTO mRNA Expression in Extremely Obese and Type 2 Diabetic Human Omental and Subcutaneous Adipose Tissues

Fat mass and obesity-associated protein (FTO) gene expression is known to correlate with obesity. Our aim was to investigate the FTO gene expression in paired omental and subcutaneous human adipose tissues from morbid and obese patients. To understand the role of CD68-positive macrophages in adipose tissues, the correlation with adiposity parameters such as adipocyte diameter and adipocyte radius was also measured. Drug and adiposity correlations were also analyzed. Paired omental and subcutaneous adipose tissue were excised during elective surgery from morbidly obese (n = 9) and obese (n = 5) patients. FTO expressions were determined by quantitative PCR. Tissue sections were analyzed for their CD68 protein expressions by immunuhistochemistry. Omental and subcutaneous adipose tissue FTO gene expression levels were not found to differ significantly among morbidly obese and obese study groups. Serum aspartate aminotransferase e and alanine transaminase levels were found to be in negative correlation with subcutaneous fat tissue FTO expression rate. Antidiabetic drug use was found to be in correlation with adiposity. Both subcutaneous and omental fat cell diameters were found to have correlation with antidiabetic drug use. Omental fat cell diameter was found to enlarge together with omental CD68 protein expression. Subcutaneous macrophage number decreased while omental fat cell radius increased. Omental macrophage number was found in correlation with subcutaneous macrophage number. Antidiabetic therapy was found to increase adiposity in omental and subcutaneous fat. Further research is needed with larger samples to explore the exact role of FTO in obesity.

Fat mobilization in water restricted Awassi ewes supplemented with vitamin C

The current study was designed to assess the effect of water restriction on fat metabolism in Awassi ewes orally supplemented with different levels of vitamin C. Experiment 1 (24 days) included four groups, four animals in each, with one group as control receiving daily water. The three remaining groups were watered once every four days, with the third and fourth groups receiving a daily oral dose of 3 g and 5 g vitamin C, respectively. Experiment 2 (21 days) was similarly designed except that the last group was administered one 10 g vitamin C oral dose at the beginning and at the middle of the experiment. Water restriction induced a reduction in feed intake and consequently weight loss in both experiments. Fat cell diameter, insulin, leptin, T3 and T4 concentrations tended to decrease in water restricted animals with or without vitamin C, while fatty acids and cholesterol increased. The observed changes reflect fat mobilization in water restricted Awassi ewes, which seemed to be correlated with insulin and leptin levels. Furthermore, fat mobilization reflected by high fatty acid and low leptin concentrations seemed to be more enhanced by daily supplementation of vitamin C than by the singular high dosages repeated twice, however further research is needed to confirm this observation.

Type-1 Diabetes Induces Depot-Specific Alterations in Adipocyte Diameter and Mass of Adipose Tissues in the Rat

Type-1 diabetes (T1D) is a metabolic disorder associated with massive reduction in mass of adipose tissue. Measuring cell diameter, an index of fat metabolism, we determined depot-specific alterations in weight of adipose tissue, fat cell diameter and size heterogeneity and distribution at 5 depots in streptozotocin (STZ)-induced diabetic rats. T1D was induced by a single injection of STZ. Seven days after the injection, fat depots were isolated, weighted, washed and maintained in tissue culture medium. Using a microscope equipped with calibrated micrometer, cell diameter as well as size distribution pattern and heterogeneity of adipocytes were determined in fresh tissue slices of subcutaneous (SC), proximal epididymal (PE), distal epididymal (DE), perirenal (PR) and retroperitoneal (RP) fat depots. The T1D induced marked reductions in fat mass and mean of fat cell diameter at all depots. The most affected depot was the SC. With the exception of PE, adipocytes at all depots showed significant increases in size heterogeneity. The effect of the diabetes on mean fat cell diameter and size heterogeneity was minimal at PE depot. Depots with similar cell size distribution pattern exhibited similar fat mass reduction. However, the DE depot with a unique cell size distribution pattern showed a fat mass reduction similar to that of PE and PR depots. These data indicate that T1D induces a massive fat mass reduction in a reasonably depot-specific manner and that the fat depots close to survival organs are less vulnerable to fat mobilization. Moreover, peculiar disagreement between cell size distribution and heterogeneity as well as the level of fat mass reduction at DE and PE depots suggests that not only cell size and heterogeneity but also local factors may play roles in depot-specific fat mobilization.

Effects of monoclonal antibody on fat tissue development, carcass composition, growth performance and fat metabolism of pigs by subcutaneous injection

This study was to investigate the effects of monoclonal antibody against a porcine 40-kDa adipocyte-specific plasma membrane protein on fat tissue development, carcass composition, growth performance and fat metabolism in pigs. Forty-eight Landrace × Saba pigs were randomly divided into eight groups, the control group was given 16 mL saline and the treat groups were given the monoclonal antibody (McAb) with 0.1, 0.5 or 1.0 mg/kg body weight at 30 kg or 60 kg body weight respectively by subcutaneous injection. The results showed that the injection of 1.0 mg/kg monoclonal antibody at 30 kg or 60 kg could increase the lean meat percentage by 3.04% or 4.25% ( P < 0.05) respectively, decrease fat percentage by 10.50% or 9.32% ( P < 0.05) and backfat thickness by 16.28% or 18.65% ( P < 0.05) respectively under the condition of unchanged growth performance. Moreover, the injection of 1.0 mg/kg monoclonal antibody at 30 kg body weight could significantly increase serum LPL activities by 13.79%, 25.00%, 43.91%, 21.77% and 11.61%( P < 0.05) at 1 to 5 weeks respectively after injection, increase serum TG contents by 7.83%, 11.08% and 5.37% ( P < 0.05) at 2 to 4 weeks respectively after injection, but reduce serum NEFA levels by 6.58%, 7.80% and 8.15%( P < 0.05) at 1 to 3 weeks respectively after injection. The injection of 1.0 mg/kg monoclonal antibody at 60 kg body weight could significantly increase serum LPL activities by 10.02%, 18.77% and 14.26%( P < 0.05) at 1 to 3 weeks respectively after injection, increase serum TG contents by 9.23%, 9.70% and 8.67%( P < 0.05) at 2 to 4 weeks respectively after injection, but reduce serum NEFA levels by 15.46%, 16.64%, 13.96% and 10.85%( P < 0.05) at 1 to 4 weeks respectively after injection. Meanwhile, this antibody could restrain subcutaneous fat tissue development by reducing the diameter and triglyceride contents of subcutaneous fat cells. This suggested that this McAb could improve the carcass composition by reducing fat percentage which was regulated by increasing fat mobilization and suppressing the fat deposition in adipose tissue.

Effects of glucocorticoid on adipocyte size in human bone marrow

The pathogenesis of corticosteroid-induced femoral head necrosis is assumed to be related to lipid metabolism. Mature fat cells are believed to play a central role in lipid metabolism. The purpose of this study was to investigate the size of mature fat cells in the human femoral head after steroid treatment. Cancerous bone tissue was obtained from the femoral heads of 20 women who had undergone total hip arthroplasty. This bone tissue was subsequently incubated in a medium containing 10(-7) or 10(-5) M dexamethasone for 5 days. Mature fat cells from the bone marrow were observed by scanning electron microscopy, and the largest diameter of individual fat cells was measured. The size of the mature fat cells in human bone marrow increased after high-dose steroid treatment. The largest fat cell volume after steroid treatment was one and one-half times larger than that observed in the control. Steroid-induced osteonecrosis is known to sometimes occur after high-dose steroid treatment. These findings may indicate the pathogenetic factors in the early stage of steroid-induced osteonecrosis.

Platelet and endothelial cell-derived microparticles in steroid-induced osteonecrosis of the femoral head of rabbit model

To explore the relationship between the alterations of platelet-derived microparticles (PMPs) and endothelial cell-derived microparticles (EMPs) and steroid-induced osteonecrosis of the femoral head. Forty-four adult Japanese white rabbits were randomly divided into 2 groups: experimental group (n = 44), injected intramuscularly once with 20 mg/kg of methylprednisolone acetate, and control group (n = 28) injected with normal saline of the same dose. Blood samples were collected from the auricular vein while the animals were in a fasting state in early morning prior to experiment (week 0), and 2, 4, and 8 weeks after the injection. The levels of prothrombin time (PT), activated partial prothrombin time (APTT), and anti-thrombokinase-III (AT-III) were examined. Plasma was ultra-centrifuged and the circulating platelet and EMPs were isolated to undergo flow cytometry to detect the amounts of CD31, CD42a, CD54, and CD62E. 1, 2, 4, and 8 week after the injection 6 rabbits from the experimental group and 4 rabbits from the control group were sacrificed respectively and their femoral heads were taken out to undergo histopathologic examination with HE staining and microthrombus and elastic fiber staining. The PT, APTT, and AT-III levels increased significantly 1 to 8 weeks after the injection. The numbers of EMPs and PMPs were also increased markedly after steroid administration. Histopathologic examination demonstrated an accumulation of bone marrow cell debris, presence bone empty lacunae in the trabeculae 1 week after the steroid injection. 2, 4, and 8 weeks after the steroid injection the bone necrosis was remarkable, fatty degeneration of bone marrow cells occurred, the diameter of fat cells increased, and the area ratio of fatty cells became higher. MSB staining was positive. High dose glucocorticosteroid increases the levels of PMPs and EMPs that may be related to hypercoagulability and thrombosis in microcirculation and play an important role in steroid-induced osteonecrosis. MP can be considered a true target in the pharmacological control of steroid-induced osteonecrosis.

Effect of the detraining status on high-fat diet induced fat accumulation in the adipose tissue and liver in female rats

The purpose of the present study was to investigate the effects of a high-fat diet (HFD) in previously trained rats that have been detrained for different periods. Two groups of female rats were, first, either treadmill trained for 8 weeks or remained sedentary (Sed). Trained animals, thereafter, remained inactive for 4 weeks (Inact-4 weeks), while fed a standard diet, before being submitted to a high-fat diet (42% kcal of fat) for an additional 2 or 6 weeks. The order was reversed in a 3rd group in which rats were first kept sedentary for 4 weeks before being submitted to the same 8-week training program that ended with the initiation of the HFD (Inact-0 week). Fat accumulation in the mesenteric depot ( P < 0.05) and in the sum of 3 intra-abdominal (urogenital, retroperitoneal, and mesenteric; P = 0.065) tissues in response to the HF feeding was higher in trained rats kept inactive for 4 weeks than in Sed and Inact-0 week animals. Liver triacylglycerol accumulation also showed a tendency to be higher ( P < 0.07) in Inact-4 weeks than in Inact-0 week rats. These changes were not associated with significant changes in fat cell diameter and number in the mesenteric adipose tissue. When rats in all groups were subdivided into obesity prone (OP) and obesity resistant (OR) on the basis of the change in body weight gain in response to the HFD, liver lipid infiltration was higher ( P < 0.01) in OP Inact-4 weeks rats than in all other groups. The present results indicate that previously trained rats that have been inactive for a while maintain higher body adiposity in response to a HFD than in freshly inactive and sedentary rats.

Effects of ingesting a high-fat diet upon exercise-training cessation on fat accretion in the liver and adipose tissue of rats

The purpose of the present study was to determine if exercise trained rats might benefit from protection against fat accumulation in response to an obesity stimulus initiated upon training cessation. Two groups of female rats were either treadmill trained for 8 weeks (DTr) or remained sedentary (Sed). They were then submitted either to a high-fat diet (HF; 42 E%) or kept on a standard diet (SD; 12.5 E% lipids) for another 6 weeks while remaining sedentary. Fat accumulation in liver and adipocytes along with fat-cell diameter and plasma free fatty acid (FFA) levels were measured 0, 2, and 6 weeks after training cessation. Immediately after the training period (t = 0), DTr rats exhibited similar body mass and higher dietary intake but smaller body fat content (4 fat pads) compared with Sed rats. DTr rats, under both diets, exhibited higher gains in body fat than Sed rats (DTr vs. Sed, 71% vs. 8% and 132% vs. 55% for SD and HF, respectively), such that fat mass in all 4 depots was similar to Sed rats 6 weeks after training cessation. Despite higher adipocyte fat accretion, liver lipid infiltration was not increased in DTr animals and plasma FFA levels were lower throughout the detraining period. In addition, plasma leptin levels remained lower in DTr animals throughout the detraining period under the HF diet condition. The present results indicate that previously exercise trained rats are not protected against adipocyte fat accumulation whether they ingest a standard or a high-fat diet.