Adipose Tissue Of Male Rats Research Articles

Developmental plasticity in sympathetic nervous system response to fasting in adipose tissues of male rats

While fasting suppresses sympathetic nervous system (SNS) activity in most peripheral tissues, the response of sympathetic nerves in white adipose tissue (WAT) is reportedly stimulatory. To confirm this finding and to determine if the fasting response in WAT is susceptible to developmental modification, SNS activity was compared in fed and fasted animals using techniques of [ 3H]norepinephrine ([ 3H]NE) turnover. Studies were performed in commercially reared 7-week-old male rats, in male rats reared in the local vivarium, and in male rats reared until 30 days of age at either 18°C or 30°C. In commercially reared animals, [ 3H]NE turnover was elevated in epididymal fat during the second day of fasting, a response not seen during the preceding or succeeding day of fasting. On the other hand, in rats reared from birth in the local vivarium a 1-day fast led to suppression of SNS activity in epididymal fat. In rats reared at 18°C for the first 30 days of life, fasting suppressed SNS activity in retroperitoneal fat in contrast to the absence of this response noted in 30°C-reared rats. These studies demonstrate that sympathetic responses in WAT to fasting in young adult, male rats are susceptible to modification by the environmental conditions present during the first month of life.

Trophic Effects of Menhaden Fish Oil in Female Rats

Previous studies have demonstrated growth inhibition of adipose tissue in male rats fed high-fat diets supplemented with fish oil. Whether or not similar effects are observed in females is unknown. Our lab is currently investigating the hypothesis that adiposity in female rats may be limited by feeding high-fat diets containing menhaden fish oil. Methods: 52 female Sprague-Dawley rats (175–200g) were fed one of two high-fat diets (20% by weight), containing either corn oil (CO) or menhaden fish oil (MFO) as the primary source of dietary fat. Animals were sacrificed at 0, 6, 12, 20, and 32 weeks to determine dietary-associated changes in adiposity over time. Body weights and fat depot weights (inguinal, parametrial, mesenteric, and retroperitoneal) were recorded across all time points. Results: Overall, there was a significant treatment effect of diet upon both body weight and weight gain (2-way ANOVA, P<.001); a greater increase in weight was observed in MFO-fed animals. At specific time points, MFO groups gained significantly more weight than CO-fed animals as recorded at 12 and 20 weeks (P<.05). However, no differences in weights of the individual fat depots relative to body weight were observed. There were no significant differences in food intake. Conclusions: Greater weight gain in MFO-fed rats with proportional increases in fat depot weights implies a stimulatory effect upon overall body growth rather than specific effects upon adipose tissue. In contrast to earlier studies in male rats, adiposity in female rats is not limited by feeding menhaden fish oil as a source of dietary fat. Our results suggest that caution must be exercised in interpreting experimental data from dietary studies across genders.

Effects of Dexamethasone on Primarily Cultured Newly Differentiated Rat Adipocytes from Different Adipose Tissue Regions

The effects of dexamethasone (dex) on newly differentiated adipocytes in primary culture derived from mesenteric, retroperitoneal, epididymal, and inguinal subcutaneous adipose tissues of male rats were studied. The degree of differentiation was similar in these adipose precursor cells derived from different regions as assessed by lipoprotein lipase (LPL) activity, an early marker of adipocyte differentiation. LPL activity was increased by addition of dex, and no differences in degree of activation were observed in cells from different adipose tissue regions. Development of both basal and isoproterenol-stimulated lipolysis was also similar in adipose precursor cells from different adipose tissue regions. Dex addition enhanced the isoproterenol-stimulated lipolysis with no regional differences. Studies of binding of [3H]-dex showed no regional differences in either binding affinity or maximal binding capacity. It is concluded that dex stimulates both LPL activity and lipolytic activity in newly differentiated rat adipocytes in primary culture. This seems, however, not to vary in magnitude in cells obtained from different adipose tissue regions. This might be due to the apparent similarity of number and affinity of glucocorticoid binding sites. Regional variations in glucocorticoid regulated LPL and lipolytic activity in adipose tissue might therefore not be due to inherent differences between adipocytes.

Effects on animal growth and lipid composition of heart, liver, and adipose tissue in male rats fed different levels and types of fats.

Weanling male rats were fed diets containing 5, 10, or 20% (by weight) fat. Diets were made isocaloric by decreasing the amount of starch as the diet fat level increased. At each fat level, three oil mixtures were fed which contained 13, 32, or 79% saturated fatty acids. The polyunsaturate level was 11% of total fatty acids in all mixtures. After 12 weeks, animals eating the high fat diets had gained significantly less weight and had eaten less feed. These animals also had significantly lighter livers and more liver lipids. The level and type of fat in the diet affected the amount (mg/g) of several phospholipids in the liver and heart. The fatty acid patterns (total saturates, n - 3, n - 6 fatty acids) of the major phospholipids were generally constant, the monounsaturated fatty acids being the major exception.

A 24-hour fast-induced loss of energetic substrates in the interscapular brown adipose tissue of ‘cafeteria’ rats

The incorporation of tracer-labelled glucose and alanine, as well as the levels of energetic components in interscapular brown adipose tissue of male rats fed either standard or ‘cafeteria’ diet have been studied in fed and 24-hour of food withdrawal situations. The relative amount of brown adipose tissue in cafeteria fed rats was much greater than in controls, whose size and composition were not altered with food withdrawal. Cafeteria fed rats lost significant amounts of both lipid and protein during food withdrawal. Label incorporation was comparable for glucose and alanine except within the lipidic fraction, in which cafeteria fed rats showed a considerably lower efficiency. The loss of protein with food withdrawal and the swift incorporation of alanine into protein, tissue amino acid pools and lipids suggest an easy utilization of these amino acids by both groups of rats. In addition, the loss of energetic substrates observed in the cafeteria fed rats during food withdrawal suggests a continued utilization of energetic substrates by this brown adipose tissue, a condition not observed in the tighter energetic budget of control rats.

Prolonged Effects of Fasting-Refeeding on Rat Adipose Tissue Lipoprotein Lipase Activity: Influence of Caloric Restriction during Refeeding

We studied lipoprotein activity in white adipose tissue of male rats during a 3-day fast and up to 21 days of refeeding. Changes in LPL were considered in relation to concomitant changes in fat cell size. During fasting fat cell size decreased and LPL activity declined markedly (80%). With ad libitum refeeding LPL activity returned to control values by 3 or 5 days of refeeding, increased above control values (60–100%) by 10 days of refeeding and returned to control values by 20 days of refeeding. The normalization and overshoot of LPL activity preceded and accompanied increases in fat cell size, wich occurred between days 5 and 10 of refeeding; LPL activity returned to control values only after fat cell size also returned to control values. Mild food restriction (approximately 25%) during refeeding allowed LPL activity to return to control values but reduced the magnitude and duration of the overshoot. Severe food restriction (approximately 50%) during refeeding delayed the return of LPL activity to control values until day 20 of refeeding. These data support a role for LPL in restoration of adipocyte lipid stores during refeeding. Food restriction during refeeding influences LPL and may modulate the rate of lipid accumulation by adipocytes during refeeding.

In vivo changes in the rates of total lipid and fatty acid synthesis in liver and white adipose tissues of male rats during postweaning growth

1. 1. In suckling rats, lipid synthesis is low in liver and adipose tissues. The rest of carcass is the major site of body lipogenesis. 2. 2. After weaning, lipid synthesis (per g of wet wt) strongly increases in liver, penrenal and subcutaneous adipose tissues, and rest of carcass. The relative contributions of liver and both adipose tissues to body lipogenesis are about 35–40 and 6–9% respectively, but the rest of the carcass is still the main site of lipogenesis up to the age of 50 days. 3. 3. In adult rats, lipid synthesis (per g of wet wt) remains high in liver but is strongly reduced in adipose tissues and carcass. Liver becomes the principal site of body lipogenesis.

Exercise and the cAMP system in rat adipose tissue II. Nucleotide catabolism.

In this study the effect of exercise training on the adenosine 3',5'-cyclic monophosphate (cAMP) system of rat adipose tissue has been investigated. The basal amount of cAMP for the exercising rats was 0.179 +/- 0.021 nmol/10(6) cells, the same value as for the controls. Phosphodiesterase activities (low and high Km) remained unaffected as a result of the program of treadmill running. Kinetic constants for the low- and high-Km phosphodiesterases revealed that the affinity of the enzymes for substrate (cAMP) was unaltered by physical training. Finally, ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid, possibly through its effect on calmodulin, stimulated or inhibited (depending on concentration) phosphodiesterase activity in the same direction and to a similar extent in extracts of adipose tissue from runners and controls. Taken together, these data clearly demonstrate the exercise training has no effect on the cAMP system of adipose tissue in male rats.

Effects in the Rat of Environmental Temperature, Diet Dilution, and Treadmill Running on Liver and Adipose Enzymes and Metabolism of 14C-Glucose: A Multiple Regression Analysis

The effects of two environmental temperatures (T; 16 degrees and 31 degrees), five diet dilutions (D; 0%, 12.5%, 25%, 37.5% and 50%), and five daily treadmill running periods (E; 10 minutes, 40 minutes, 70 minutes, 100 minutes, and 130 minutes) upon enzyme activities of liver and adipose tissue of male rats were observed. Liver enzymes studied were glucose-6-phosphatase (G6Pase), 6-P-gluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), fructose diphosphatase (FDPase), NADP-isocitrate dehydrogenase (ICDH), and malic enzyme (ME). Adipose tissue (epididymal fat) enzymes (6PGD, G6PD, and ME) were studied as well as the in vitro incorporation of the 14C of [U-14C] glucose into liberated 14CO2 and into the triglycerides, free fatty acids, and total lipids by adipose tissue slices. Equations describing regression surfaces for these responses (expressed as units/100 g body weight) could contain significant linear coefficients of the independent variables (T, D, and E), their first order interactions, and quadratic coefficients for D and E. Significnat regression coefficients for activities of liver enzymes associated with increased lipogenesis (6PGD, G6PD, and ME) produced response surfaces with conformations generally concave downward. All enzymes possessed positive and negative linear and quadratic coefficients for D which caused response surfaces to be concave downward with respect to that variable. Also, 6PGD and G6PD (positive linear and negative quadratic coefficients for E) exhibited response surfaces concave downward with respect to E. Additionally, 6PGD showed greater activity at 31 degrees than at 16 degrees while G6PD showed no effect of temperature on activity. Liver ICDH, probably important in supplying reducing equivalents for fatty acid synthesis, evidenced response surfaces almost identical to those for 6PGD. Significant regression coefficients for activity of liver enzymes associated with increased gluconeogenesis (FDPase and G6Pase) produced for FDPase a response surface concave downward with respect to both D and E with greater values at 31 degrees than at 16 degrees; but for G6Pase non-concave surfaces with lesser values at 31 degrees than at 16 degrees. Significant regression coefficients for activities of adipose enzymes associated with increased lipogenesis produced for 6PGD a response surface concave upward due to negative linear and positive quadratic coefficients for both D and E. For G6PD and ME regression surfaces were concave upward with respect to E, but these were modified by positive and negative linear coefficients, respectively, for D. Significant regression coefficients for incorporation of the 14C of glucose into triglycerides and free fatty acids of adipose tissue slices and their production of 14CO2 yielded response surfaces concave upward with respect to E (negative linear and positive quadratic coefficients). In addition, the surface for free fatty acids was concave upward with respect to D. The 14CO2 production was greater at 16 degrees than at 31 degrees...

Studies on Atherosclerosis : II. Clinical Investigation on Lipid Mobilizer

The author reported in the preceding paper (Studies on Atherosclerosis : Part 1) that the combined administration of lanolin and lipid mobilizer induces marked lipemia as well as atherosclerosis in the rabbits. Studies on lipid mobilizer (LM) in man have been reported by clinical findings with the quantitative changes of LM. The author attempted to measure the amount of LM in the human blood serum and to clearify its part in the development of atherosclerosis. Material and Methods 1) In vitro measurement of LM. LM was obtained and purified after Seifter's method from 2ml of the blood serum obtained from the hungry patients in the early morning. The amount of serum LM was evaluated according to its character to inhibit the activity of lipoprotein lipase. 0.3ml of lipoprotein lipase solution was added with 0.3ml of 10% human albumin solution (pH 8.5), 0.3ml of lipid mobilizer solution and 4.0ml of diluted cow's milk (1 in 600, dilutant : 0.25M NH3-NH4Cl, pH 3.5 diluted three times with saline), and incubated at 37°C for two hours. After the procedure the turbidity was compared. 2) Purification of lipoprotein lipase. Periepididymal and perirenal adipose tissue of male rats were put in the cold acetone (O°C, 30 times as much as the tissue), and homogenized at O°C, and then centrifuged in 6000 rpm for 20 minutes. The supernate was discarded. The precipitate was repeatedly washed in cold acetone and ether, and then dried under the decreased pressure in low temperature. This stock powder was dissolved in 0.025M NH3NH4Cl buffer solution (pH 8.6) at O°C and left for 60 minutes, and centrifuged in 8000 rpm for 30 minutes, and then the supernate was diluted in a proper way every time for use. 3) Preparation of anti-β-lipoprotein. Human blood serum containing a large amount of β-lipoprotein was added with 20 times as much volume of 4mg/dl dextran sulfate in physiological saline solution containing sodium citrate. 15-60 minutes later, this mixture was centrifuged in 6000 rpm for 30 minutes. The supernate was discarded. The same procedure was repeated 5 or 6 times to get the pure β-lipoprotein. 15-20 mg dose of this preparation was injected in to the rabbit subcutaneously 15 times. After the procedure, anti-β-lipoprotein-seurm was obtained. This serum reacted specifically with β-lipoprotein to form a single precipitation zone in agar gel double diffusion method (after Ouchterlony). 4) Patients with coronary disease, hypertension and cerebrovascular disease were subjected to this experiment. Healthy adult persons were examined as the control.