Activity In White Adipose Tissue Research Articles

Effect of acute cold exposure on norpinephrine turnover rates in rat white adipose tissue

The present studies were carried out to assess directly sympathetic activity in white adipose tissue in response to cold exposure. Norepinephrine (NE) content and NE turnover rates were determined in epididymal and retroperitoneal adipose tissue from rats exposed to cold (4°C and controls kept at ambient temperature. Parallel measurements were made in interscapular brown adipose tissue (IBAT), in which activation of catecholaminergic innervation by cold exposure is well known. Exposure to 4°C for 4 h reduced the endogenous NE content by 50% in MAT and by 30% in both epididymal and retroperitoneal adipose tissues. Compared to warm controls, average values of fractional rates of turnover and of turnover rates, estimated with α-methyl-tyrosine, increased 5-fold in IBAT and 2.5-3-fold in epididymal and retroperitoneal tissues from rats exposed to cold. The present data provide the first direct evidence that white adipose tissue sympathetic activity is increased during acute cold exposure.

The effects of a selective Alpha-1 adrenergic blockade on the activity of adipose tissue lipoprotein lipase in female hamsters

Lipoprotein lipase, is an enzyme responsible for the hydrolysis of triacylglycerols at the surface of endothelial cells. Its regulation is not completely elucidated and seems, among other things, under the influence of the sympathetic nervous system. The adrenergic regulation of lipoprotein lipase activity is complex and the α 1 adrenergic pathway appears involved in this regulation. In the present study, adipose tissues of female hamsters are investigated following a single injection of doxazosin and phenylephrine and are compared to controls for the activity of lipoprotein lipase. After an acute treatment with a selective α 1 antagonist (doxazosin), lipoprotein lipase activity was decreased in the parametrial white adipose tissue and increased in brown adipose tissue (p <- 0.05). Moreover, a treatment with phenylephrine,' an α 1 adrenergic agonist, increased the activity of lipoprotein lipase, in the parametrial fat pad only. On the other hand, the activity of lipoprotein lipase in heart and in skeletal muscle was not modified by an α 1, stimulation or blockade. In this study, calcium and norepinephrine did not appear involved in the regulation of lipoprotein lipase activity. On the contrary, the increase of plasma glycerol after an acute treatment with doxazosin suggests that the lipolytic activity of white adipose tissue could be involved in the decrease of lipoprotein lipase activity in the parametrial white adipose tissue.

Anti-Tumour Necrosis Factor-α Treatment Interferes with Changes in Lipid Metabolism in a Tumour Cachexia Model

1. Rats bearing the Yoshida ascites hepatoma AH-130 showed an important decrease in white adipose tissue lipoprotein lipase activity as compared with non-tumour bearing rats. This was associated with a lower adipose tissue mass, as estimated from the weight of the lumbar fat-pads. Conversely, lipoprotein lipase activity was markedly increased in brown adipose tissue and heart. 2. These changes were associated with a distinct hyperlipaemia, essentially manifested as an increase in circulating triacylglycerol levels, whereas no changes were observed in glycaemia. 3. Tumour-bearing rats were treated with a polyclonal anti-murine tumour necrosis factor-alpha antibody or with a non-immune IgG preparation. Control animals were either untreated or received a non-immune IgG preparation. Anti-tumour necrosis factor-alpha treatment resulted in a significant increase in lipoprotein lipase activity in white adipose tissue in animals bearing a tumour growing exponentially (day 4 after inoculation) as compared with the animals receiving a non-immune goat IgG preparation. In addition, animals bearing an stationary tumour (day 7 after inoculation) and submitted to anti-tumour necrosis factor-alpha treatment had a higher adipose tissue lipoprotein lipase activity as compared with the IgG- or the non-treated groups. Correspondingly, circulating triacylglycerol levels were markedly decreased, with a lower hyperlipaemia than in control tumour-bearing rats. 4. These observations suggest that tumour necrosis factor-alpha is involved in activating the lipid metabolic changes that develop in rats after transplantation of a fast-growing tumour.

Effects of tri-iodothyronine administration on the disposal of oral [1-14C]triolein, lipoprotein lipase activity and lipogenesis in the rat during lactation and on removal of the litter

The effect of tri-iodothyronine (T3) administration on the utilization of dietary [14C]lipid by the mammary gland and adipose tissue of lactating and litter-removed rats was studied. (1) After an oral load of [1-14C]triolein, the lactating rats treated with T3 (50 micrograms/100 g body wt.) over 24 h showed an increase in 14CO2 production and a decrease in the total [14C]lipid transferred through the mammary gland that was paralleled by a decrease in tissue lipoprotein lipase (LPL) activity. (2) T3 administration decreased plasma prolactin in the lactating rats. Prolactin replacement in T3-treated rats restored LPL activity in the mammary gland, but did not increase the amount of dietary [14C]lipid transferred to the milk. (3) Chronic T3 administration (4 days) to lactating rats did not affect pup growth or the lipogenic rate in the mammary gland. (4) The administration of T3 to litter-removed rats inhibited the increase of LPL activity in white adipose tissue and decreased the accumulation of dietary [14C]lipid. This decrease was accompanied by increased 14CO2 production and [14C]lipid accumulation in skeletal muscle and heart. (5) It is concluded that hyperthyroidism depresses LPL activity in mammary gland and white adipose tissue, but not in muscle. The increased accumulation of [14C]lipid in muscle and increased production of 14CO2 in lactating and in litter-removed rats treated with T3 is in part due to the decreased total LPL in mammary gland and adipose tissue respectively, which are therefore less able to compete with muscle for the available plasma triacylglycerols.

Inhibition of lipogenesis in rat brown adipose tissue by clofibrate

The effect of clofibrate (Atromid S, ethyl-2-(4-chlorophenoxy)-2-methylpropionate) administration for 7 days to rats on lipogenesis and on some lipogenic enzyme activities in brown adipose tissue (BAT), liver and white adipose tissue (WAT) was examined. As compared to control rats the rate of lipogenesis in BAT in the clofibrate-treated animals was significantly decreased. The rate of liver lipogenesis increased slightly, whereas lipogenesis in the WAT was not affected by clofibrate. In BAT, the drug treatment resulted in depression of fatty acid synthase, ATP-citrate lyase, malic enzyme, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities. The activity of liver fatty acid synthase did not change, ATP-citrate lyase activity slightly decreased, whereas the activity of malic enzyme significantly increased in this organ after clofibrate feeding. The ATP-citrate lyase activity in WAT decreased, while fatty acid synthase and other lipogenic enzymes were not changed after clofibrate feeding. Clofibrate treatment did not influence the activity of NADP-linked isocitrate dehydrogenase and malate dehydrogenase (enzymes not linked directly to lipogenesis), either in BAT, liver or WAT. The data presented suggest that the hypolipidaemic effect of clofibrate in the rat may be due (possibly among other mechanisms) to reduction of the rate of fatty acid synthesis in BAT but not in the liver and WAT.

Chronic intracerebroventricular neuropeptide-Y administration to normal rats mimics hormonal and metabolic changes of obesity.

Chronic intracerebroventricular (icv) administration of neuropeptide-Y (NPY; 10 micrograms/day) was performed in normal female rats to investigate its hormonal and metabolic consequences. Intracerebroventricular NPY produced hyperphagia, increased basal insulinemia, as well as liver and adipose tissue lipogenic activity. It also increased basal morning corticosteronemia. When NPY-induced hyperphagia was prevented by pair-feeding, the icv NPY treatment resulted in the same increases in basal insulinemia and corticosteronemia, and liver and white adipose tissue lipogenesis was still higher than that in respective controls. Under the ad libitum and pair-feeding conditions, icv NPY stimulated glucose uptake as well as total lipoprotein lipase activity in white adipose tissue; it resulted in an increase total activity of hepatic and white adipose tissue acetyl coenzyme-A-carboxylase. As all hormonal and metabolic changes elicited by icv NPY remained present (at the same or to a lesser extent depending upon the parameter considered) when hyperphagia was prevented by pair-feeding, it was, thus, shown that icv NPY per se induces peripheral hormonal and metabolic alterations via efferent routes, which remain to be determined. The effects of icv NPY reported in this study are similar to the defects observed in the early phase of genetic obesity in rodents, the hypothalamus of which has increased NPY levels. NPY could, thus, be of relevance in the occurrence of genetically induced obesity.

Energy balance and lipid metabolism in transgenic mice bearing an antisense GCR gene construct.

Energy balance and lipid metabolism were investigated in transgenic mice bearing an antisense glucocorticoid receptor (GCR) gene construct that impairs the normal expression of the GCR gene. Food intake was recorded during the 15 days preceding decapitation of adult normal and transgenic mice, and feces were collected to derive the digestible energy intake. Body composition measurements consisted of the determination of energy, protein, and fat content of the carcass. Carcass energy was determined by bomb calorimetry, whereas carcass protein was measured by the Kjeldahl procedure. Energy expenditure was estimated from the continuous oxygen consumption (VO2) monitoring over a 24-h period. Lipoprotein lipase (LPL) activity was quantified in epididymal white adipose tissue (WAT), heart, and vastus lateralis muscle (VLM) by measuring the in vitro hydrolysis of labeled triolein in the presence of tissue homogenates. Norepinephrine (NE) content of both interscapular brown adipose tissue (BAT) and heart were determined by high-performance liquid chromatography (HPLC). Energy intake and expenditure were significantly lower in transgenic mice than in controls. Concurrently, both fat content and total energy of the carcasses were significantly higher in the transgenic animals. In comparison with normal mice, heart and VLM LPL activity was significantly reduced in transgenic mutants. There was no difference between groups in LPL activity in WAT. Finally, heart and BAT NE contents were lower in transgenic animals than in control mice. These results suggest that a defective GCR system may affect energy balance through increasing energetic efficiency, and they emphasize the modulatory effects of hypothalamic-pituitary-adrenal axis changes on muscle LPL activity.

Lipid Deposition and Use by Black-Tailed Prairie Dogs, Cynomys ludovicianus, in the Natural Environment

Fatty acid synthase (FAS) activity was measured in black-tailedprairie dogs (Cynomys ludovicianus), nonhibernators or facultative hibernators, to compare their enzyme activity associated with fattening to that reported earlier (Turner et al. 1989) in Richardson's ground squirrels (Spermophilus richardsonii), obligate hibernators. In both species nearly all FAS activity was in white adipose tissue (WAT). Maximum FAS actiuity/mg of protein in WAT occurred after reproduction in both species and was about three times as great in ground squirrels as in prairie dogs. When rate of fat deposition was at its peak (June-August in ground squirrels, fall in prairie dogs), total FAS in WAT in ground squirrels was tuwice that in prairie dogs. Richardson's ground squirrels deposited approximately 9 g of lipid/wk during peak fattening (Turzner et al. 1989) versus approximately 5 g of lipid/wk in prairie dogs. These observations support the hypothesis that obligate hibernators fatten more rapidly than nonhibernators. During 3 wk of cold in the uwinter of 1990-1991 (air temperature less than -20° C), prairie dogs lost 30% of body weight, nearly, all of uwhich wuas lean body mass. Lipid mass was depleted during the reproductizve season, from March through June. As a result of this observation, the following year lipolytic actiuity, in liver, WAT, and brown adipose tissue (BAT) as well as body and tissue masses was measured monthly in freeroaming prairie dogs. Liver and WAT were the principal sites of lipolytic activity. Although 1991-1992 uwas not as severe as the previous winter, use of lipid stores was similar. Fat deposits remained inztact through fall and early winter, and lipolytic actizvity was louw inl all tissues. Reproductive activity began in February and March in males and females, respectively. Betuween January and March lipolytic activity in liver tripled inz both sexes. During the same period lipolytic activity in WAT doubled in females and quadrupled in males. During the reproductive season males lost 85% and females lost 91% of lipid stores. Black-tailedprairie dogs foraged throughout the year but during severe cold remained underground and catabolized primarily lean body mass. Lipolytic activity and amount of lipid present supported the hypothesis that lipid reserves are conserved through winter and supply energy for reproduction.

Alpha-1 Adrenergic Blockade Interacts with Dietary Carbohydrates on Triacylglycerol Metabolism in Rats

The purpose of this study was to evaluate the effects of prazosin, an alpha-1 adrenergic antagonist, on determinants of triacylglycerol metabolism in rats fed chronically diets high in starch or sucrose. Hepatic triacylglycerol secretion rate (HTGSR), lipoprotein lipase in white and brown adipose tissues, red vastus lateralis muscle and heart, as well as serum triacylglycerol concentration, were assessed in the post-prandial state, after injection of prazosin or saline. Post-prandial triacylglycerolemia was higher in the sucrose-fed than in the starch-fed rats. After the injection of prazosin, triacylglycerol concentrations were decreased in both dietary groups. This effect was more marked in sucrose-fed than in starch-fed rats (diet x blocker interaction: P < 0.0003). HTGSR was higher in rats fed sucrose than in starch-fed rats (+49%, P < 0.01). Prazosin decreased HTGSR (-45%) in the sucrose-fed rats but not in animals fed starch. Lipoprotein lipase activities in brown adipose tissue, vastus lateralis muscle and heart in rats injected with prazosin were enhanced compared with those of the saline-treated rats, but no change was found in enzyme activity in white adipose tissue. This effect of prazosin was independent of the type of diet. These results suggest that prazosin reduced serum triacylglycerol concentrations after food ingestion at least partly by enhancing lipoprotein lipase activity in several tissues. In addition, the prazosin-induced decrease in HTGSR in sucrose-fed rats, which was absent in starch-fed animals, probably accounted for the greater magnitude of the hypotriacylglycerolemic effect of the blocker in animals given sucrose.

Expression and regulation of the human GLUT4/muscle-fat facilitative glucose transporter gene in transgenic mice.

To study the molecular basis of tissue-specific expression of the GLUT4/muscle-fat facilitative glucose transporter gene, we generated lines of transgenic mice carrying 2.4 kilobases of the 5'-flanking region of the human GLUT4 gene fused to a chloramphenicol acetyltransferase (CAT) reporter gene (hGLUT4[2.4]-CAT). This reporter gene construct was specifically expressed in tissues that normally express GLUT4 mRNA, which include both brown and white adipose tissues as well as cardiac, skeletal, and smooth muscle. In contrast, CAT reporter activity was not detected in brain or liver, two tissues that do not express the GLUT4 gene. In addition, the relative levels of CAT mRNA driven by the human GLUT4 promoter in various tissues of these transgenic animals mirrored those of the endogenous mouse GLUT4 mRNA. Since previous studies have observed alterations in GLUT4 mRNA levels induced by fasting and refeeding (Sivitz, W. I., DeSautel, S. L., Kayano, T., Bell, G. I., and Pessin, J. E. (1989) Nature 340, 72-74), the regulated expression the hGLUT4[2.4]-CAT transgene was also assessed in these animals. Fasting was observed to decrease CAT activity in white adipose tissue which was super-induced upon refeeding. These alterations in CAT expression occurred in parallel to the changes in endogenous mouse GLUT4 mRNA levels. Although CAT expression in skeletal muscle and brown adipose tissue was unaffected, the endogenous mouse GLUT4 mRNA was also refractory to the effects of fasting/refeeding in these tissues. These data demonstrate that 2.4 kilobases of the 5'-flanking region of the human GLUT4 gene contain all the necessary sequence elements to confer tissue-specific expression and at least some of the sequence elements controlling the hormonal/metabolic regulation of this gene.

Insulin receptor kinase activity in muscles and white adipose tissue during course of VMH obesity.

Early after lesion of the ventromedial hypothalamus nuclei (VMH), insulin-induced glucose utilization is increased in white adipose tissue (WAT), whereas oxidative and glycolytic muscles are, respectively, normoresponsive or resistant to insulin. Five weeks later, all of the muscles are resistant, whereas WAT returns to normal responsiveness. The aim of this study was to characterize the insulin receptor kinase activity in WAT and muscles 1 and 6 wk after lesion. The number and affinity of insulin receptors were not modified in any of the tissues studied. Autophosphorylation and phosphorylation of an exogenous substrate were similar in oxidative and glycolytic muscles of VMH and control rats both 1 and 6 wk after the lesion. Insulin receptors from WAT of 1-wk VMH rats exhibited a 2.5-fold increase in insulin-stimulated autophosphorylation and phosphorylation. Six weeks after the lesion, both autophosphorylation and phosphorylation returned to normal values. This suggests that insulin receptor tyrosine kinase activity does not play a significant role in the insulin resistance of skeletal muscles but has a crucial role in mediating the variations of insulin action on WAT observed during the development of VMH obesity.

Adipose tissue lipolytic activity and urinary catecholamine excretion in cold-acclimated piglets

This study was designed to investigate the effect of chronic cold exposure (12 degrees C for 3 weeks) on catecholamine production and noradrenaline-induced lipolytic rate to further describe thermoregulatory mechanisms in 5- to 8-week-old pigs. Lipolytic activity in white adipose tissue was assessed in vitro while catecholamine production was estimated by measuring noradrenaline, adrenaline, and dopamine levels in 24-h urine samples. Animals were fed ad libitum and food intake was 20% greater in the cold. In control piglets maintained in a 23 degrees C environment, the addition of increasing amounts of noradrenaline (10(-6), 10(-5), 10(-4) M) stimulates lipolysis (p less than 0.05) and enhances the basal lipolytic rate (5.4 mu equiv. fatty acids.120 min-1.g-1 tissue) by 2.5-, 2.7-, and 3.9-fold, respectively. Three weeks of cold acclimation had no effect on basal lipolytic rate but increased significantly noradrenaline responsiveness: incubation of subcutaneous white fat in the presence of 10(-4) M noradrenaline does increase the basal lipolytic rate by sixfold. Noradrenaline effects were maximally activated by theophylline. Daily dopamine and noradrenaline excretions (3-10 micrograms/24 h) were increased significantly (up to eightfold) after 10 days of cold acclimation. By contrast, adrenaline excretion was quite low (0.6-1.6 micrograms/24 h) and showed no significant variation with time. It is likely that these hormonal and biochemical modifications play a prominent part in the mechanism of cold acclimation in the piglet. Their significance in the development of shivering and nonshivering thermogenesis is discussed in relation to the supply of energy substrates to the fatty acid utilizing tissues and to the possible uncoupling effect of free fatty acids.

Lipoprotein lipase activity in white adipose tissue of rats subjected to exercise–rest cycles

This study was conducted to determine serum lipid levels and the activity of lipoprotein lipase in epididymal white adipose tissue of rats undergoing exercise training. During the 8-week period of treatment, one group of rats was kept sedentary and the remaining animals were exercise trained either continually (1 h of daily treadmill running) or intermittently (alternate weeks of daily running and inactivity). Exercise training, either continual or intermittent, decreased postprandial serum total and high-density lipoprotein cholesterol concentrations, which returned to sedentary levels in the intermittently trained animals following a week of rest. Lipoprotein lipase activity in whole epididymal adipose pad was lower in rats trained continually than in the sedentary group at the end of the treatment. The intermittent training program elicited large fluctuations in both the specific (per milligram of protein) and total (per tissue) activity of lipoprotein lipase in white adipose tissue. During rest periods, enzyme activity rose to levels that were higher than those of sedentary rats, whereas lipase activity was below that of sedentary animals following a week of running. In the last exercise--rest cycle, body weight gain of the intermittently trained rats was nearly abolished during the week of running, but it increased above that of sedentary animals during weeks of rest. The present results suggest that the modulation of lipoprotein lipase activity in white adipose tissue is one of the adaptations that take place to accommodate the fluctuations in the rate of energy deposition that occur in the rat during an intermittent training program.

Attenuation of the Meal-Induced Increase in Plasma Lipids and Adipose Tissue Lipoprotein Lipase by Guar Gum in Rats

This study was designed to evaluate the effect of guar gum on the postprandial increase in plasma lipids, insulin and lipoprotein lipase (LPL) activity in white adipose tissue (WAT). Male rats were given ad libitum access to purified diets containing either no fiber or 5% guar gum for 3 wk. The animals were killed at various times after a meal (10% of daily ad libitum intake of their respective diets). Consumption of guar gum resulted in smaller final body weight (-7%, P less than 0.05) and ad libitum food intake (-10%, P less than 0.05). The difference in epididymal WAT weight induced by the concomitant diet was relatively larger (-29%, P less than 0.05) than that of whole body weight. Although no difference was seen in fasting plasma total and high density lipoprotein cholesterol levels between dietary groups, the postprandial increase in these variables was larger in the animals given the fiber-free meal than in those receiving the fiber-supplemented meal (P less than 0.01). Guar also attenuated the postprandial rise in plasma triacylglycerols. The presence of fiber in the meal reduced the postprandial increase in plasma insulin (P less than 0.01). The meal-induced rise in LPL activity of WAT was significantly smaller (P less than 0.02) in the animals fed the diet containing fiber than in those receiving the fiber-free diet. Thus, guar gum altered the activity of LPL in WAT, an effect that may be related to the insulin response to this dietary component.(ABSTRACT TRUNCATED AT 250 WORDS)

Whole-Body Lipids and Fatty Acid Synthetase Activity in Richardson's Ground Squirrels, Spermophilus richardsonii

Whole-body lipids andfatty acid synthetase (FAS) activity of liver, white adipose tissue (WAT), and brown adipose tissue (BAT) infield-caught Richardson's ground squirrels were measured to determine the effects of reproduction on fattening. Whole-body lipids increased by 9 g and 8 g/wk, respectively, in males and nonparous females between April 1 and June 5 and by 10 g/wk between May 10 and July 1 inparous females. Males were always heavier than nonparous females, but thepercentage of body mass that was lipid was similar. The lipid mass accumulated by parous females by July 1 had been achieved by nonparousfemales 1 mo earlier. For both liver and WAT, FAS activity in males and nonparous females was similar throughout the active season. FAS activity of liver was depressed in late pregnancy. FAS activity of both liver and WAT was depressed during lactation, being 70 times greater in WAT of nonparous than of parous females. FAS activity in WAT and liver of postlactating females increased, but there was no compensatory increase in rate of fattening or FAS activity above that in males and nonparous females. Apparently, parous females hibernate later than other adults because reproduction causes them to initiate fattening later, and, once initiated, rate offat deposition is similar to that in other members of the population. WAT appears to be the principal tissue of fatty acid synthesis for prehibernation fattening.

Effects of cimaterol, a beta-adrenergic agonist, on lipid metabolism in rats

Rats fed a high carbohydrate diet containing 10 or 100 ppm cimaterol for 4 weeks gained 41% to 59% less fat and 70% to 76% more protein than controls, with no major changes in either energy gain or efficiency of energy retention. Effects of cimaterol on lipid metabolism in these rats were assessed. Cimaterol stimulated lipolysis in vivo and in vitro, but failed to influence rates of de novo fatty acid synthesis in either liver or white adipose tissue. Activities of fatty acid synthetase and malic enzyme in these tissues were also unaffected by cimaterol. Cimaterol administered in vivo failed to affect lipoprotein lipase activity in white adipose tissue, but elevated enzyme activity 67% to 75% in the extensor digitorium longus muscle. Lipoprotein lipase activity in the extensor digitorum longus muscle was also elevated by 66% during a 2 hour incubation with 1 mmol/L cimaterol. We conclude that cimaterol selectively stimulates both lipolysis in white adipose tissue and lipoprotein lipase activity in skeletal muscle, to direct energy away from adipose tissue deposition toward skeletal muscle accretion.

Fatty acid synthetase in control, starved and refed Richardson's ground squirrels

1. 1. Starvation for 6 days reduced whole body mass and total body lipids to 76 and 71%, respectively, of pre-starvation levels in weight-gain phase ground squirrels. After 4 days of refeeding, body mass increased to 86% of pre-starvation level but total body lipids had not changed from starvation levels. 2. 2. Compared to the fed state, fatty acid synthetase (FAS) activity in white adipose tissue (WAT) was 15 and 31% in starved and refed 4-day animals, respectively, and in liver was 26 and 21% in starved and refed 4-day animals, respectively. Lipids depleted by starvation during prehibernatory fattening were not rapidly restored in Richardson's ground squirrels. 3. 3. Changes in these parameters with starvation and refeeding were similar in weight-loss phase animals. 4. 4. In control animals of both phases, WAT accounted for at least 90% of total FAS activity and liver nearly all of the remainder.

Lipoprotein lipase in white and brown adipose tissues of exercised rats fed a high-fat diet.

The combined effects of a high-fat-supplemented diet and exercise training on serum lipids as well as on lipoprotein lipase activity in white and brown adipose tissues of the rat were evaluated. Male Wistar rats were fed ad libitum either a stock diet or the stock diet supplemented with food items rich in fat. Half of each dietary group was submitted to daily treadmill running for 35 days. Food intake and final body weight were raised by the high-fat-supplemented diet and lowered by exercise training. Postprandial serum triglycerides were not affected by diet or exercise, whereas the latter decreased total cholesterol in the high-fat group only (14%, P less than 0.01). Total lipoprotein lipase activity in white adipose tissue was elevated (120%, P less than 0.01) by high-fat feeding, and this increase was greatly reduced by concomitant exercise training. In brown adipose tissue, however, the large elevation (104%, P less than 0.01) in enzyme activity brought by the high-fat diet was unaltered by concomitant training. Thus a high-fat-supplemented diet increased lipoprotein lipase activity in both an energy-storing and a heat-producing tissue, and exercise training was able to counteract this effect in white, but not in brown, adipose tissue. These findings support the notion that the regulation of lipoprotein lipase is tissue specific.

Tissue-specific effects of rapid tumour growth on lipid metabolism in the rat during lactation and on litter removal

1. The effect of tumour burden on lipid metabolism was examined in virgin, lactating and litter-removed rats. 2. No differences in food intake or plasma insulin concentrations were observed between control animals and those bearing the Walker-256 carcinoma (3-5% of body wt.) in any group studied. 3. In virgin tumour-bearing animals, there was a significant increase in liver mass, blood glucose and lactate, and plasma triacylglycerol; the rate of oxidation of oral [14C]lipid to 14CO2 was diminished, and parametrial white adipose tissue accumulated less [14C]lipid compared with pair-fed controls. 4. These findings were accompanied by increased accumulation of lipid in plasma and decreased white-adipose-tissue lipoprotein lipase activity. 5. In lactating animals, tumour burden had little effect on the accompanying hyperphagia or on pup weight gain; tissue lipogenesis was unaffected, as was tissue [14C]lipid accumulation, plasma [triacylglycerol] and white-adipose-tissue and mammary-gland lipoprotein lipase activity. 6. On removal (24 h) of the litter, the presence of the tumour resulted in decreased rates of lipogenesis in the carcass, liver and white and brown adipose tissue, decreased [14C]lipid accumulation in white adipose tissue, but increased accumulation in plasma and liver, increased plasma [triacylglycerol] and decreased lipoprotein lipase activity in white adipose tissue. 7. The rate of triacylglycerol/fatty acid substrate cycling was significantly decreased in white adipose tissue of virgin and litter-removed rats bearing the tumour, but not in lactating animals. 8. These results demonstrate no functional impairment of lactation, despite the presence of tumour, and the relative resistance of the lactating mammary gland to the disturbance of lipid metabolism that occurs in white adipose tissue of non-lactating rats with tumour burden.

Concomitant food intake and adipose tissue responses under chronic insulin infusion in rats

Body weight (BW), food intake (FI), and activity of white adipose tissue (WAT) and brown adipose tissue (BAT) were studied in adult male rats under chronic insulin infusion. Insulin was infused for 4, 7 or 10 days via implanted minipumps. Insulin-treated rats gained more BW than control rats until the 7th day of infusion. At 10 days, the difference in BW decreased. The average cumulative FI was significantly higher after 4, 7 and 10 days of insulin infusion. Feed efficiency (FE) was increased in insulin-treated rats after 4 and 7 days. An increase in WAT weight was observed in insulin-treated rats together with an increased activity of lipogenic enzymes. BAT weight was augmented after 4 days of insulin infusion. This was due mainly to lipid accumulation. Specific mitochondrial guanosine diphosphate (GDP) binding was significantly decreased by 58% in insulin-treated rats after 4 days of infusion. This reduced thermogenic activity, along with the increased FI and FE were responsible for the rapid BW gain observed during the first 7 days of insulin infusion.