Influence of the beta 2-adrenergic agonist clenbuterol on insulin-stimulated lipogenesis in mouse adipocytes

Growing mice fed the beta 2-adrenergic agonist clenbuterol (CB; 20ppm) had increased rate of growth and altered composition of gain (greater protein and less fat). Adipocytes prepared from the epididymal fat pads of treated and untreated mice were used to examine the influence of CB on lipid metabolism. Using cells from untreated mice, CB stimulated lipolysis to an equivalent maximum rate as epinephrine (EPI), but CB was far less potent (EC50 (microM); CB = 5, EPI = 0.2). Both CB and EPI inhibited insulin-stimulated lipogenesis over the physiological range of insulin concentrations. This inhibition was expressed as a dose-dependent decrease in tissue sensitivity to insulin and a decrease in maximal lipogenic capacity. Inhibition of maximal rate, but not of insulin sensitivity, could be stimulated by the addition of palmitate without EPI or CB. Adipocytes isolated from CB-treated mice did not differ from controls in sensitivity to insulin or in activity of fatty acid synthetase. Increased lipolysis and reduced lipogenesis as observed in vitro with CB are consistent with reduced fat accretion in CB-treated mice. However, the absence of detectable changes in adipocyte lipogenesis from CB-fed mice leaves open the question of the relevance of altered lipid metabolism to the observed changes in body composition.     

Acute effects of beta-adrenergic agonists on porcine adipocyte metabolism in vitro

Backfat was obtained at slaughter from market weight hogs to study the acute effects of clenbuterol (CB), ractopamine (RAC) or epinephrine (EPI), in the presence and absence of theophylline (THEO) or adenosine deaminase (ADA), on rates of lipolysis and fatty acid synthesis in vitro. Only EPI increased lipolytic rate in the absence of THEO or ADA. In the presence of THEO or ADA, RAC and CB were lipolytic, although CB had a lower maximal response. With THEO present, RAC and EPI increased lipolysis with a similar potency and responsiveness. Lipolytic responses from all agonists were prevented by propranolol. Insulin stimulated glucose incorporation into fatty acids 50 to 100%; stimulated rates were not influenced by any agonist, either alone or in the presence of ADA. When THEO was present, EPI and RAC inhibited fatty acid synthesis approximately 50%. Clenbuterol was not inhibitory under any conditions. Results indicate that, under appropriate conditions, beta-adrenergic agents increase lipolysis and decrease lipogenesis in porcine adipocytes. Combined evidence suggests that lipolysis is more sensitive to beta-adrenergic stimulation than is insulin-stimulated lipogenesis. Finally, RAC and CB possess only partial agonist activity relative to EPI, CB being least active.     

Myostatin null mice respond differently to dietary‐induced and genetic obesity

Our objective was to determine sensitivity of myostatin null (MN) mice to obesity induction by dietary or genetic means. To induce dietary obesity, 3‐week‐old wild type (WT) and MN mice were fed diets with 60% calories (HF) or 10% calories from fat (LF) for 4 weeks. MN mice did gain body fat on the HF diet but to a lesser extent than WT mice. Body weight and fat content was similar in MN mice fed HF and LF diets. To induce genetic obesity, the MN mutation was incorporated into leptin db/db (DB) mice generating mice homozygous for each mutation (MNDB). Nine‐week‐old MNDB mice were obese, similar to DB mice. Body weight, body fat content, fat pad weight and adipocyte size were all increased in MNDB mice compared to MN and WT mice and were quite similar to DB mice. However, fasting blood glucose, an indicator of insulin resistance and diabetes, was reduced in MNDB mice compared to DB mice. These results indicate that MN mice gain less body fat than WT on a HF diet, but the MN mutation does not alter fat accumulation caused by DB mutation. Thus, MN mice are not always resistant to obesity development.     

Effects of the beta-adrenergic agonist L644,969 on muscle protein turnover, endogenous proteinase activities, and meat tenderness in steers.

Eight MARC III composite (1/4 Hereford, 1/4 Angus, 1/4 Pinzgauer, and 1/4 Red Poll) steers weighing approximately 350 kg were fed 0 or 3 ppm of the beta-adrenergic agonist L644,969 (Merck Sharp and Dohme Laboratories, Rahway, NJ) for 6 wk in a high-concentrate diet. Feed efficiency was higher (P less than .05) in beta-adrenergic agonist-fed steers at 1, 3, 5, and 6 wk on trial. Average daily gain was greater (P less than .05) in beta-adrenergic agonist-fed steers at 3, 5, and 6 wk on treatment. Fractional degradation rate (percentage/day) of skeletal muscle myofibrillar protein was 27.1% lower (P less than .05) in beta-adrenergic agonist-fed steers at 3 wk on trial. Fractional accretion rate (percentage/day) of skeletal muscle myofibrillar protein in beta-adrenergic agonist-fed steers was higher (P less than .05) at 1, 3, 5, and 6 wk on trial. The beta-adrenergic agonist-fed steers had heavier (P less than .05) carcasses (9.6%), larger (P less than .05) longissimus muscle areas (24.3%), and lower (P less than .05) USDA yield grades (43.8%). Marbling degree, USDA quality grade, kidney, pelvic, and heart fat percentage, and 12th rib fat thickness were not different (P greater than .05). Calpastatin activity was higher (P less than .05) in muscle from the beta-adrenergic agonist-fed steers at 0 and 7 d postmortem. There were no differences (P greater than .05) in mu- or m-calpain or in cathepsins B or B+L or cystatin(s) between beta-adrenergic agonist-fed and control steers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sensitivity of lipolysis and lipogenesis to dibutyryl-cAMP and beta-adrenergic agonists in swine adipocytes in vitro

The sensitivities of lipolysis and fatty acid synthesis to dibutyryl-cAMP (dbcAMP), epinephrine, ractopamine and clenbuterol were quantified in vitro using porcine adipocytes. Insulin-stimulated lipogenesis showed a biphasic response to dbcAMP, with increased rates at low concentrations and decreased (55%) rates at higher concentrations of dbcAMP. In the absence of insulin, lipogenesis was inhibited 78% by dbcAMP. In the presence of adenosine deaminase or theophylline, all three beta-adrenergic agonists inhibited basal lipogenesis, but only epinephrine and ractopamine inhibited insulin-stimulated lipogenesis. The relationship between suppressed lipogenesis and enhanced lipolysis in response to dbcAMP and the beta-agonists revealed that 1) basal lipogenesis was more sensitive to inhibition than was the stimulation of lipolysis, 2) sensitivity differences were magnified if adenosine deaminase was present and 3) insulin decreased adipocyte sensitivity to the inhibitory effects of dbcAMP and the beta-adrenergic agonists. These results indicate that the relative sensitivities of lipogenesis and lipolysis to beta-adrenergic stimulation can be modified by adenosine and insulin. Furthermore, adenosine and insulin antagonize beta-adrenergic responses, in part, by cAMP-independent mechanisms.     

Incorporation of dietary polyunsaturated fatty acids into pork fatty tissues.

The incorporation and elimination rate of dietary PUFA in pork fat was investigated in this study. Experiment 1 examined the incorporation of dietary PUFA into backfat (BF) and into the triglyceride (TG) and phospholipid (PL) fractions of the i.m. fat of the loin. Experiment 2 examined the elimination of PUFA from BF due to withdrawal of PUFA from the diet. In Exp. 1, Piétrain x Seghers Hybrid pigs (70 barrows and 70 gilts averaging 11 wk of age and 30 kg initially) were assigned to five dietary treatments in a 2 x 5 factorial arrangement during a 16-wk feeding period. Pigs received a diet containing about 2.5% tallow (T) for 8, 10, 12, 14, or 16 wk, followed by a diet containing about 15% full-fat soybeans (FFS) for 8, 6, 4, 2, or 0 wk, respectively. Additionally, BF biopsies were taken every 2 wk from eight pigs on the 8-wk FFS dietary treatment, starting from the time pigs were switched to the FFS diet. Linoleic acid [18:2(n-6)], linolenic acid [18:3(n-3)], eicosadienoic acid [20:2(n-6)], arachidonic acid [20:4(n-6)], and PUFA contents in BF increased (P < .01) with time on the FFS diet, but contents of these fatty acids were similar for pigs fed FFS for 6 or 8 wk. The PUFA content of the biopsies rose throughout the FFS treatment; the greatest increase in PUFA occurred during the first 2 wk of feeding FFS. The PUFA content of the TG and PL fractions in i.m. fat of the longissimus muscle tended to increase with time on the FFS diet. The increase was significant (P < .01) in the TG fraction for 18:3(n-3) and in the PL fraction for 20:4(n-6) and 22:6(n-3). In Exp. 2, 11-wk-old pigs (10 barrows and 10 gilts) were fed a FFS-based diet from 11 to 19 wk of age, followed by the T-diet for an additional 8 wk. During the latter period, biopsies were taken every 2 wk. The elimination of PUFA from BF was greatest during the first 2 wk after the dietary change. The PUFA reached the lowest level at the age of 25 wk. These experiments show that the PUFA: saturated fatty acid ratio of BF can be increased from .34, corresponding with a T-based diet, to .55, by feeding a FFS diet for 6 wk before slaughter.     

The effect of increasing photoperiod and food restriction in sexed broiler-type birds. I. Growth and abdominal fat cellularity.

1. Sexed broiler-type chicks were raised either under a continuous (CON) 23 h Light (L) and 1 h Dark (D) schedule or an increasing photoperiod (INC) consisting of an initial 6 h L and 18 h D which increased by 4 h L per week from 14 to 35 d of age after which a 23 L:1D was maintained to 49 d of age. 2. From 5 to 11 d of age birds were fed either: ad libitum (AL), energy intake (kJ ME) restricted to 9.414 x gBW0.67 (R1) or energy intake (kJ ME) restricted to 6.276 x gBW0.67 (R2). Food intake was ad libitum at all other times. 3. Food restriction reduced growth to 49 d of age although some compensatory growth did occur. Food efficiency was not significantly affected by restriction. 4. Although abdominal fat pad weight was significantly reduced for R2 compared to AL, this was not significant on a percentage body weight basis. 5. Adipocyte number in the abdominal fat pad was similar for AL, R1 and R2, but concomitant with a smaller fat pad weight, R2 showed reduced adipocyte volume compared to AL. 6. INC birds were lighter at 21 d of age, but body weights were equivalent to CON by 42 d of age. 7. Abdominal fat pad weight was some 10% larger at 49 d of age for INC birds. Adipocyte volume was unaffected, the increase in adipocyte being entirely caused by an increase in adipocyte number in INC birds.     

Determination of the affinity of ractopamine and clenbuterol for the beta-adrenoceptor of the porcine adipocyte

Dissociation constants (Kd) of ractopamine and clenbuterol for the swine adipocyte beta-adrenergic receptor were estimated from competition studies with epinephrine for the stimulation of lipolysis. Both compounds competitively inhibited epinephrine-stimulated lipolysis in the absence of adenosine deaminase. Three methods for estimating Kd values were used and similar estimates were obtained with each method. Ractopamine and clenbuterol showed greater affinity for the beta-receptor than did epinephrine and had similar Kd values of 1 to 2 x 10(-7) M. The low capacity of ractopamine and clenbuterol to stimulate lipolysis in vitro does not result from poor coupling to the beta-receptor. Ractopamine and clenbuterol may be considered partial agonists, possessing high affinity for the beta-adrenoceptor but exhibiting a relative ineffectiveness for adenylate cyclase activation.     

Effect of cimaterol on sheep adipose tissue lipid metabolism

Effects of dietary cimaterol (5 mg/kg) on adipose tissue metabolism of wether lambs were studied. Lipogenesis, lipolysis, fatty acid composition and adipocyte size and number were measured. Cimaterol feeding increased lipogenesis; however, this effect was not statistically significant. Insulin (1,000 microU/ml) stimulated lipogenesis of adipose tissue from control sheep. However, this elevated rate was abolished by in vitro cimaterol. Insulin had no stimulatory effect on lipogenesis in cimaterol-fed sheep. Lipolysis was depressed by cimaterol feeding. However, 10(-4) M cimaterol stimulated lipolysis in the adipose tissue from both control and cimaterol-fed sheep. Insulin inhibited stimulated lipolysis in adipose tissue from control sheep but had no effect on the stimulated lipolysis in cimaterol-fed sheep. Mean adipocyte diameter was smaller (from 74 to 70 microns) and adipocyte size distribution also was changed in the cimaterol-fed sheep. Adipocyte number per gram of tissue was not affected by cimaterol. There was a significant increase in percentage of unsaturated fatty acids in adipose tissue from cimaterol-fed sheep. These results indicate that lipogenic and lipolytic responses to insulin and cimaterol in sheep adipose tissue were altered by cimaterol feeding. The carcass fat content decrease in cimaterol-fed sheep may be attributed to the reduction in adipocyte size.     

Effect of swine weaning age on body fat and lipogenic activity in liver and adipose tissue

Two experiments were conducted to evaluate the effects of weaning swine at 2 or 5 wk of age on postweaning performance and fat metabolism. In the first experiment, 52 pigs were weaned at 2 or 5 wk of age with body weights determined from birth to 8 wk. The early weaned group was fed a 20% protein corn-soybean meal-oat diet containing 25% dried whey from 2 to 5 wk while both groups were fed a 20% protein cereal grain-based diet from 5 to 8 wk of age. In a second experiment, a total of 90 pigs weaned at similar ages and fed the same diet sequences were killed at weekly intervals from 2 to 8 wk of age to evaluate body fat content and lipogenesis in liver and adipose tissue. Lipogenic capacity was measured by incorporation of acetate-1 14C into the total lipid fraction in liver slices and adipose tissue minces or by monitoring liver ATP citrate lyase activity. The results demonstrate that pigs weaned at 2 wk experience a slower postweaning growth rate with lower empty body weights than those either concurrently nursing the dam or weaned at 5 wk of age. Both groups had similar body weights from 6 to 8 wk of age. The body fat content of nursing pigs increased from 2 to 5 wk of age. Pigs weaned at 2 wk lost approximately 25% of their body fat the first week postweaning while later-weaned pigs did not lose body fat postweaning. Body fat composition of both groups was similar by 8 wk of age. Lipogenic activity was higher in liver than in adipose tissue from 2 to 5 wk of age and remained relatively constant throughout the trial. Adipose tissue lipogenic activity was lower in the nursing pig but increased dramatically at 5 wk in the early-weaned group and 7 wk of age in the late weaned group. These results suggest that weaning age can affect postweaning body fat composition and that adipose contributes a greater lipogenic capacity than liver tissue as the pig matures.     

Experiments to optimize enzyme substitution therapy in pancreatic duct-ligated pigs

Ligation of the pancreatic duct in pigs leads to severe maldigestion and malabsorption of crude nutrients. Supplementation with 24 capsules of Creon (Solvay Pharmaceuticals GmbH, Hannover, Germany) per meal led to an increased digestibility of crude nutrients. With regard to optimization of the treatment of EPI no essential improvements can be achieved by adding omeprazol or lecithin to the diet. In pancreatic duct-ligated pigs the isolated addition of omeprazol led to an increase of the pre-caecal digestibility of crude fat and organic matter. With additional enzyme substitution, the application of omeprazol did not result in an improved fat digestibility. Isolated addition of lecithin to the diet resulted in a reduced total digestibility of crude fat. Offering the diet twice a day and using a higher frequency of enzyme applications (four or six instead of only two applications) had no effects on the digestibilty of crude fat or organic matter. According to the observations in pancreatic duct-ligated pigs, the addition of missing enzymes to the diet led to the best treatment results in EPI. Administration of omeprazol or a higher feeding frequency as well as the application of enzymes in small proportion of the whole meal or dosages given consecutively over the day showed no advantages. Furthermore, the present study suggests that the addition of lecithin cannot be recommended in EPI, when given diets with butter as the predominant fat source as in human dietetics.     

Effects of additional starch or fat in late-gestating high nonstarch polysaccharide diets on litter performance and glucose tolerance in sows

The effects of feeding additional starch or fat from d 85 of gestation until parturition on litter performance and on glucose tolerance in sows that were fed a diet with a high level of fermentable nonstarch polysaccharides (NSP) were studied. The day after breeding, 141 multiparous sows were assigned to the experiment. At d 85 of gestation, sows were assigned to the treatments. Sows were fed 3.4 kg/d (as-fed basis) of a high-NSP diet or the same quantity of the high-NSP diet and an additional 360 g of starch (from wheat starch) daily, or the same quantity of the high-NSP diet and an additional 164 g of fat (from soybean oil) daily. During lactation, all sows were given free access to the same lactation diet. Approximately 1 wk before the expected time of parturition, an oral glucose tolerance test was performed in 38 randomly chosen sows by feeding pelleted glucose (3 g/kg BW0.75). Blood samples for glucose analyses were taken at -10, 10, 20, 30, 40, 50, 60, 70, 80, 90, 105, and 120 min after glucose was fed. The supply of additional dietary starch or fat did not increase piglet birth weight or total litter weight at birth. Sows that were fed the high-NSP diet had more (P = 0.097) live-born piglets and fewer (P = 0.084) stillborn piglets than did sows that were fed additional fat, whereas sows that were fed additional starch were intermediate for these variables. Piglet mortality after birth was not affected by dietary treatment. Body weight and backfat gains in the last month of gestation were higher for sows fed additional starch or fat than for sows fed the high-NSP diet (P < 0.001 and P = 0.017, respectively). Feed intake in lactation was greatest by sows fed the high-NSP diet, least by sows fed additional starch at the end of gestation, and intermediate by sows fed additional fat (P = 0.099). The differences in lactation feed intake did not result in differences in BW and backfat losses during lactation. Sows that were fed additional fat had the greatest glucose area under the curve (P = 0.044), indicating that these sows were less tolerant to glucose. In conclusion, feeding additional energy (starch or fat) in late-gestating sows that are fed a high-NSP diet did not increase litter weight at birth or piglet survival, but did increase maternal gain. Feeding sows additional energy from fat might induce glucose intolerance, whereas feeding sows additional energy from starch did not induce glucose intolerance.     

Site of administration and duration of feeding oleamide to cattle on feed intake and ruminal fatty acid concentrations

Two experiments were conducted to determine effects of oleamide on feed intake and ruminal fatty acids when the oleamide was introduced in the feed vs through a ruminal fistula (Exp. 1) or the oleamide was fed for an extended (9-wk) length of time (Exp. 2). In Exp. 1, four nonlactating Holstein cows, each fitted with a ruminal cannula, were fed four diets in a 4 x 4 Latin square design. Each period lasted 2 wk. Diets consisted of 48% corn silage and 52% concentrate on a DM basis. One diet contained no added fat (control) and a second diet contained 4.2% oleic acid. The remaining two diets were designed to expose cows to 4.2% amide (as oleamide) either through the feed (AF) or by administering oleamide into the rumen (AR) each day through the ruminal cannula. The AF diet reduced DMI similarly to results reported previously for lactating dairy cows and sheep. Intake of the oleic acid diet was intermediate between the control and AF diets. Dry matter intake was reduced by AR similarly to the AF diet. The acetate:propionate ratio in samples of ruminal contents was reduced by oleic acid but not by AF or AR. In Exp. 2, 12 steers were divided into three equal groups of two Angus and two Simmental x Angus crosses, and each group was assigned a diet containing either no added fat (control), 4% oleamide, or 4% high-oleic canola oil. All steers had ad libitum access to feed and water. Dry matter intake by steers fed the canola oil diet was not different from that by steers fed the control diet when averaged over the first 3 wk, the last 3 wk, or over the entire 9-wk study. Oleamide reduced DMI 4 kg/d over the first 3 wk of the study. However, DMI of the oleamide diet consistently increased over the 9-wk study, resulting in wk 7 to 9 DMI that was not different from that of steers fed the control diet. These results show that the reduction in feed intake when oleamide is added to cattle rations can be attributed more to physiological responses than to an undesirable unique taste or odor of the oleamide. In finishing beef steers, the decreased intake induced by oleamide was most severe during the first 1 or 2 wk of feeding but gradually lessened over time until it nearly returned to normal by wk 9.     

Weekly digestibilities of diets supplemented with corn oil, lard or tallow by weanling swine

Two experiments were conducted to evaluate supplementation of diets with 8% corn oil, lard or tallow. In Exp. 1, 36 barrows weaned at 21 d of age were used to evaluate the effects of these three diets on digestibilities of fat and dry matter and subsequent N retentions from wk 1 to 4 postweaning. In Exp. 2, 147 weanling pigs in six replicates were used to evaluate weekly growth and feed performance measurements when fed these same diets for a 4-wk postweaning period. A large quantity of fat was absorbed (P less than .01) during wk 1 postweaning by pigs fed the corn oil diet, with the quantity absorbed similar for the three sources of fat from wk 2 to 4. Diets with corn oil had a higher apparent fat digestibility than diets supplemented with lard or tallow during each week postweaning (P less than .05). Apparent digestibility of fat increased (P less than .01) for each fat source each week postweaning but appeared to reach a plateau by wk 3 postweaning. Differences in apparent digestibility of fat between fat sources narrowed from wk 1 to wk 4, with digestibility of corn oil increasing from 79 to 89% and of animal fat sources increasing from 67 to 84%. Apparent digestibility of dry matter tended (P less than .10) to be highest when corn oil was provided during the initial 2-wk postweaning period. Although N retention was highest during wk 1 postweaning when the corn oil was fed, this response was attributed to the higher feed intakes of pigs fed this diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of isoprothiolane and phytosterol on lipogenesis and lipolysis in adipocytes from rats of dietary fat necrosis

To study effects of isoprothiolane and phytosterol on dietary fat necrosis, 3 groups of rats were fed hardened-tallow (HT) diet. Two groups of rats received either isoprothiolane (50 mg/kg) or phytosterol (20 mg/kg) orally once a day consecutively for 10 weeks. One group of rats received standard diet (CE-2) as a control. Fat necrotic lesions were observed in epididymal and perirenal adipose tissues from all rats in the 3 groups fed HT diet. Rats with fat necrosis were characterized by visceral type obesity and saturation in fatty acid composition of triglyceride in adipose tissue. The highest glucose conversion to total lipids was seen in adipocytes from the rats given phytosterol. There was no lipolytic response to epinephrine stimulation (1-100 microM) in adipocytes from the rats given only HT diet, while similar response of adipocytes from the 2 groups treated with either drug to those from the rats fed standard diet was observed. The levels of total saturated fatty acids of phospholipid in adipose tissue from the rats given either drug were lower than that of the rats given only HT diet. These data suggest that either drug alters fatty acid composition of phospholipid in fat cell membrane and enhances lipolysis of the cells.     

Alteration of body composition in rats: effect of organic chromium and L-carnitine

A growth trial was carried out to test the effect of organic, trivalent chromium and L-carnitine on the body composition of growing rats. At the same time, an evaluation of different measurement methods (weight of epididymal fat pad, adipocyte morphometry, total body electrical conductivity) was performed. Outbred Wistar rats of 30 days of age were fed diets of different (0, 10 and 20%) protein level. The diets were supplemented with 4 mg/kg Cr as chromium nicotinate, and 100 mg/kg L-carnitine. The experimental feeding lasted 15 days, after a 5-day-long adjustment period. It was found that Cr addition increased feed intake. Both treatments caused changes in body composition, increasing fat and protein deposition. Organic chromium had no effect at either protein level, while L-carnitine improved the protein retention only at an optimum (20%) protein supply. No statistically significant correlation was found between total body electrical conductivity (TOBEC) and body composition, which could be attributed to the great individual differences. A close correlation was found among total body fat percentage, weight of epididymal fat pad and the adipocyte surface. The data suggest that there is an interaction between dietary protein supply and the effect of repartitioning agents.     

Postnatal development of stearoyl coenzyme A desaturase gene expression and adiposity in bovine subcutaneous adipose tissue

This investigation addressed the hypothesis that stearoyl coenzyme A desaturase (SCD) gene expression would serve as a postnatal marker of adipocyte differentiation in bovine s.c. adipose tissue. Samples of tailhead s.c. adipose tissue were obtained by biopsy from preweaning steer calves 2.5 wk, 5 mo, and 7.5 mo of age and from yearling steers 12 mo of age. Samples also were obtained at slaughter when the steers were 18 mo of age. The steers sampled as yearlings were fed native pasture from weaning until 12 mo of age, and the steers sampled at slaughter were fed a high-concentrate diet from 12 to 18 mo of age. Major peak adipocyte volumes for the 2.5-wk-, 5-mo-, and 7.5-mo-old steers were 14, 270, and 700 pL, respectively (P < .001). The steers did not gain weight during pasture feeding, and at 12 mo of age peak adipocyte volume had decreased (P = .009) to 270 pL. At this time, a second, smaller population of adipocytes had appeared with a peak volume of 115 pL. At slaughter, adjusted fat thickness of the steers was 1.60 +/- .13 cm, the USDA yield grade of the carcasses was 3.51 +/- .31, and peak adipocyte volume had increased (P = .01) to over 2,500 pL. The number of adipocytes per 100 mg of adipose tissue doubled (P = .006) between 2.5 wk and 5 mo of age, concurrent with the nearly 20-fold increase in peak adipocyte volume, indicating that this was a period of apparent adipocyte hyperplasia. Uncoupling protein mRNA was undetectable at all stages of postnatal growth, indicating that differentiating tailhead s.c. adipocytes do not acquire brown adipocyte characteristics postnatally. Lipogenesis expressed on a cellular basis was low in all preweaning samples and increased significantly above preweaning values only in the 18-mo-old steers. Stearoyl coenzyme A desaturase mRNA concentration also was low in all preweaning samples, but it peaked (P = .07) at 12 mo of age. Because the peak in SCD mRNA concentration preceded a significant rise in lipogenesis and lipid filling, we conclude that the level SCD gene expression may be indicative of the extent of terminal differentiation in bovine tailhead s.c. adipose tissue.     

Use of carbohydrate and fat as energy source by obese and lean swine

Genetically obese and lean pigs were fed isonitrogenous-isoenergetic (digestible energy) amounts of a high or low fat diet from 25 kg body weight. Obese pigs gained less and required more feed per unit gain than lean pigs. Lean pigs were more muscular with less fat than obese pigs. Obese pigs utilized more dietary amino acids for energy (greater plasma urea N) than did lean pigs. Weight gain was similar at all intermediate periods in obese pigs fed the two diets. However, gain tended (P less than or equal to .10) to be greater and the ratio of dietary energy intake to gain tended (P less than or equal to .10) to be less in obese pigs fed high compared with low fat diets. Similar results were observed in lean pigs fed the two diets. The high fat diet produced more carcass adipose tissue deposition in both strains after 20 wk of feeding (detectable by ultrasound at 14, but not at 7 wk). Adipose tissue lipogenic rate (glucose incorporation) was similarly depressed by fat feeding in both obese and lean pigs. Obese and lean pigs both utilized dietary carbohydrate and fat differentially but there was no indication of genetic divergence regarding this utilization. In both strains of pigs, energy from the fat-enriched diet was preferentially partitioned into carcass adipose tissue.     

The effect of different high‐fat diets on erythrocyte osmotic fragility,growth performance and serum lipid concentrations in male,Japanese quail (Coturnix coturnix japonica)

Poultry diets are formulated with additional animal fat or vegetable oils to improve growth rate and feed conversion efficiency. High‐fat diet feeding in rats and fish has been shown to result in alterations in the phospholipid composition and cholesterol content of the erythrocyte membrane, in turn affecting erythrocyte osmotic fragility. In contrast, the few studies performed using high‐fat diet feeding in avian species show no changes in erythrocyte osmotic fragility. This study made use of the Japanese quail as no data exists on investigation of this species with respect to high‐fat diet feeding and erythrocyte osmotic fragility. Fifty‐seven male quail were randomly divided into six groups and fed either a standard diet (commercial poultry feed) or one of five high‐fat diets (commercial poultry feed with 22% of either coconut oil, lard, palm oil, soya bean oil or sunflower oil on a weight/weight basis) for 12 weeks. All birds on the high‐fat diets were significantly heavier (p < 0.05) after the 12‐week feeding period, than when commencing the dietary intervention. Serum triglyceride concentrations of birds in all high‐fat diet groups were significantly lower (p < 0.05) than birds in the standard diet group, whereas only birds in the palm oil group had significantly lower (p < 0.05) serum cholesterol concentrations compared to the standard diet group. Fragiligrams of erythrocytes from birds in the various dietary groups were similar. High‐fat diet feeding with different types of additional fat did not affect the osmotic fragility of the quail erythrocytes. Feeding quail high‐energy diets of varying degrees of fatty acid saturation was well tolerated and did not seem to affect the overall health status of the birds. Resistance of avian erythrocytes to modification by excess dietary fat may be a general characteristic of avian erythrocytes.