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Rats with obesity-producing, hypothalamic knife cuts (KC) were fed a purifiedhigh fat diet for 9 wk. KC rats consumed more energy ( + 70-100%) and retained energy with a much higher efficiency than control rats. Adrenalectomy of KC rats 1 wk (before gross obesity was evident) or 5 wk (when KC rats were 70% overweight) after KC surgery caused a reduction in energy intake to levels approximating those of control rats. Furthermore, energy retention in adrenalectomized KC rats was depressed more than could be explained on the basis of the reduction in energy intake. Two factors associated with the reduction in energy retention, urinary excretion of norepinephrine, an indicator of sympathetic nervous system activity, and GDP binding to brown adipose tissue mitochondria, an indicator of the thermogenic capacity of the tissue, were higher in vadrenalectomized KC rats than in pair-fed KC rats. Removal of the adrenals not only suppressed hyperphagia in KC rats fed a high fat diet, but also increased energy expenditure per kilocalorie consumed. J. Nutr. 117: 1121-1128, 1987.

SummaryPigs were pair-fed one or four meals per 48 hr for 5.5 months. Meal frequency did not influence body weight gain, body composition, glucose tolerance or plasma glucose, cholesterol or triglyceride levels. Pigs fed less frequently exhibited elevated malic enzyme activity in adipose tissue.

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16:0, oleate 18:1, or linoleate 18:2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18:2 addition to the basal diet did result in a significant (P less than 0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18:2 or linolenate 18:3 significantly (P less than 0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18:1 caused no depression in hepatic FAS activity but did result in a significant (P less than 0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18:2- or +18:3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18:3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18:2 and 18:3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis.

Rats were trained to eat a fat-free high carbohydrate diet from 800 to 1100 hours each day. After adaptation to meal-eating, the fat- free diet was supplemented with 8% methyl stA©arate(Ci8;o) or 3% methyl linoleate (Ci8:2) for 7 days. Relative to the fat-free group, hepatic utiliza tion of acetate unit equivalents (C2 units) for fatty acid synthesis per mg soluble protein by the Ci8:o group was not significantly altered, whereas Ci8:2 supplementation significantly depressed hepatic fatty acid synthesis. Supplemental Ci8:2 also caused a significant decline in liver fatty acid synthetase and acetyl CoA carboxylase while fat-free and Ci8:o groups dis played similar enzyme activities. Within a treatment, C2 unit utilization tor in vivo fatty acid synthesis was identical to that of acetyl CoA car boxylase and fatty acid synthetase activities in vitro. Therefore, shortly after a meal, the hepatic activities of these two enzymes appear to be functioning at near capacity. Ci8:2 supplementation to the fat-free diet for 7 days caused a 25% decline in glucokinase and pyruvate kinase activ ities, but only pyruvate kinase was significantly depressed. In contrast, citrate cleavage enzyme and fatty acid synthetase were both significantly reduced in activity by 50%. Plasma unesterified fatty acid levels in rats fed Ci8:2 for 5 days were not significantly elevated prior to a meal, al though dietary Ci8:2 did cause a fourfold rise in plasma free linoleate. Quantitation of long chain acyl CoA esters in freeze-clamped liver tissue of rats fed fat-free or fat-free plus 3% Ci8:2 or Ci8:3 diets revealed no con centration differences between treatments either before or after a meal. Similarly, lactate and pyruvate concentrations as well as the lactate: pyru vate ratios were not significantly changed by dietary Ci8:2 or Ci8:3. The inhibitory effects of C18:2 or Ci8;3 appear not to be mediated through changes in total plasma free fatty acid levels, in total hepatic long chain acyl CoA concentration or in hepatic cytosolic redox state. J. Nutr. 107: 1277-1287, 1977.

The nuclear content of skeletal muscles from lean and obese (ob/ob) male mice was investigated. Four lean and four ob/ob mice were examined at 2, 3, 5, 8, and 16 weeks of age. Differences in body weight between the two phenotypes were significant after 5 weeks of age. For all ages in the soleus and after 3 weeks of age in the gastrocnemius, muscle wet weight and length were less in ob/ob mice than in lean mice. Age did not influence the incidence of myonuclei in fiber cross sections for either muscle. Compared to lean mice the incidence of myonuclei per fiber cross section was significantly lower for ob/ob mice in the soleus muscle but not in the gastrocnemius muscle. The incidence of satellite cells in fiber cross sections and the percentage of nuclei within the basal lamina that were satellite cell nuclei decreased as age increased. Muscle fibers of ob/ob mice contained fewer myonuclei either because of shorter muscle length (gastrocnemius), or because of the combined effect of shorter muscle length and fewer myonuclei per unit length (soleus). The lower apparent number of myonuclei in the muscles of ob/ob mice was associated with a lower apparent number of satellite cells.

Chicks were allowed access to food for 2 hours per day (meal-fed) or were fed ad libitum. Tritiated water was administered intravenously, and the incorporation of tritium into fatty acids was used to estimate in vivo rates of fatty acid synthesis. Allowing the meal-fed chick access to a meal increased the hepatic rate of fatty acid synthesis up to 50-fold. Hepatic activities of malic enzyme and fatty acid synthetase were similar before and after the meal. The rate of fatty acid synthesis was greater in the fed meal-eater than in the ad libitum-fed chichen. Plasma free fatty acid levels were decreased and plasma triglyceride levels were increased when the meal-eater was fed. Oral and intravenous glucose tolerance tests were conducted. Meal-feeding did not impair glucose tolerance in the chicken, as has been reported in meal-fed humans. Unlike in the rat, intravenous glucose tolerance was not greatly influenced by meal pattern in the chicken. Oral glucose tolerance was improved in one of two experiments as a consequence of meal-eating. These results suggest that the chicken does respond to a shift in meal pattern.

Obese ( ob ob ) and lean mice at 4 weeks of age were housed at 23 °C or 14 °C for 4 or 8 weeks to determine effects of acclimation to mild cold on the growth of skeletal muscle, bone, and fat. Body weights at 12 weeks of age averaged 48 ± 0.6 g and 27 ± 1.9 g for obese mice housed at 23 °C and 14 °C and 29 ± 0.5 g and 26 ± 0.6 g for lean mice housed at 23 °C and 14 °C, respectively. At 23 °C, muscle weights of obese mice were approximately 60% of those in lean mice. Muscles of obese mice did not grow during the first 4 weeks at 14 °C (4 to 8 weeks of age) but did show a small gain during the second 4 weeks (9 to 12 weeks of age) at 14 °C. As a result, by the end of 8 weeks at 14 °C, muscles of obese mice weighed only 35% to 45% as much as muscles of lean mice. Growth of the tibia and femur followed the same pattern as the muscles. Obese mice housed at 23 °C from 4 to 12 weeks of age contained about six times as much fat as lean mice at this age. Although exposure to 14 °C for 8 weeks depressed the accumulation of fat in obese mice, they still contained approximately three times the percentage body fat as lean counterparts. The concentrations of corticosterone and insulin in plasma of 8 week old obese mice housed at 23 °C were two to four times and 20 times higher, respectively, than in lean mice; after 4 weeks at 14 °C the difference for corticosterone was even greater, ie, five to ten times higher in 8 week old obese, whereas the concentration of insulin in plasma of obese mice was only seven times higher than in lean mice at 14 °C. The marked reduction in skeletal muscle and bone growth observed in young obese mice as a result of cold acclimation permitted them to decrease body weight gain to equal that of lean mice without a concomitant reduction in their high percentage of body fat. These cold-induced reductions in muscle and bone growth in obese mice may have been facilitated by the observed changes in plasma corticosterone levels.

Rats were meal-fed once daily methyl esters of palmitate (Ci6:o); stA©arate(Ci8:0); linoleate (C18:2) and linolenate (Ci8:3) to de termine the influence of these fatty acids on glucokinase and fatty acid synthetase activities and on in vivo rates of fatty acid synthesis in the liver. Addition of 1% Ci6:0 or 3% C18:3to a fat-free basal diet did not alter the rate at which the diet was removed from the stomach and small intestine. Consumption of a diet containing Ci8:2 for eight meals significantly re duced hepatic fatty acid synthetase activity and in vivo rates of fatty acid synthesis by 40%, but did not alter glucokinase activity. At least three meals of a diet containing C18:2 or Ci8:3 were required to inhibit hepatic fatty acid synthesis. Conversely, after rats consumed Ci8:2, more than two meals of a fat-free diet were required to increase hepatic rates of fatty acid synthesis. Dietary C18:o and C18:0did not alter rates of fatty acid synthesis in rat liver. Glucokinase was not influenced by any of the methyl esters fed in all trials except one. The results of this study suggest that polyunsaturated fatty acids can specifically influence hepatic fatty acid syn thesis and fatty acid synthetase activity without altering glucokinase activity, and that meal-fed rats must consume at least three meals con taining polyunsaturated fatty acids before hepatic fatty acid synthesis or fatty acid synthetase activity is altered. J. Nutr. 107: 1468-1476, 1977. INDEXING

A basal diet or a basal diet plus 1% of cholesterol and 0.33% cholic acid was fed to rats for varying lengths of time and (1) the activities of liver phosphoenolpyruvate-carboxykinase (PEP-CK), tyrosine transaminase (TT), and serine dehydratase (SD); (2) the rate of total hepatic protein synthesis and (3) the concentration of hepatic reduced glutathione (GSH) were quantitated. The specific activity of PEP-CK was significantly depressed by cholesterol plus cholic acid feeding, while the specific activity of TT was unchanged. No significant effect of dietary cholesterol plus cholic acid was found on the total liver activities. In contrast, SD specific activity was increased 3-fold. The rate of (U-14C)-L-leucine incorporation into total TCA precipitable protein following ingestion of cholesterol plus acid was significantly reduced when the data were expressed as dpm (U-14C)-L-leucine/mg protein. After correcting this expression for specific radioactivity of the liver tissue free leucine pool, no significant effect of dietary cholesterol plus cholic acid on hepatic protein synthesis existed. In fact, the amount of 14C-leucine incorporated into protein on a total liver basis was 50% greater for the cholesterol group. On a per gram of liver basis, the concentration of GSH in the liver of rats fed a cholesterol plus cholic acid diet was significantly decreased. Considering the liver enlargement in rats fed cholesterol plus cholic acid, total organ GSH was found to be significantly greater than for rats fed a basal diet.

Obesity-producing, hypothalamic knife cuts and ventromedial hypothalamic (VMH) lesions in ad libitum-fed adult rats increased intake of a high-fat diet (123 and 130%) and energy retention (880 and 1,099%) during the 4-wk period postsurgery; even when pair fed to control rats, energy retention of the knife-cut and lesioned rats was still elevated (105 and 155%). Thermogenic capacity of brown adipose tissue (BAT), estimated from guanosine diphosphate (GDP) binding to BAT mitochondria, was unchanged in hyperphagic knife-cut and VMH-lesioned rats and was reduced approximately 50% when these rats were pair fed to controls. Urinary excretion of norepinephrine (NE) was approximately twofold higher in ad libitum-fed, knife-cut, and lesioned rats than in control rats; restriction of energy intake decreased NE excretion to control values. Rates of NE turnover in heart paralleled urinary NE excretion, whereas NE turnover in BAT was generally not increased in the hyperphagic rats. Urinary epinephrine excretion, an index of adrenal medullary activity, was depressed in all knife-cut and VMH-lesioned rats. Hyperphagia coupled with a lack of increased heat production in BAT causes gross obesity in ad libitum-fed, knife-cut, and VMH-lesioned rats, whereas obesity in pair-fed rats develops in part at least as a result of reduced heat production by BAT.

Obese mice, self-selecting from three food cups containing carbohydrate, fat and protein supplemented with minerals and vitamins, selected the same proportion of energy from protein (approximately 20%) as did lean mice. Young obese mice also selected the same proportion of carbohydrate and fat as selected by lean mice, but adult obese mice self-selected a higher proportion of energy from fat and a lower proportion from carbohydrate than did lean mice. The high preference by adult obese mice for fat was confirmed in additional studies employing two food cups, one containing a high-carbohydrate diet and the other a high-fat diet. We speculate that the preference by adult obese mice for fat is related to their insulin resistance.

Carbohydrate and fat are major sources of energy in the diets of many people. Carbohydrate and fat make nearly equal contributions to the energy content of the United States diet, 46 and 42%, respectively (FNB, 1974). To compare carbohydrate and fat as energy sources in a diet, replacement of one with the other must be on an equal-energy basis rather than on a weight basis. Unfortunately, reports still periodically appear in which the differences in energy values of fat and carbohydrate are not considered when the diets are formulated. The nutrient-to-energy ratio is thus altered, and it is very difficult to interpret the results.

SummaryDirect measurements of heat production were made in 3 to 4 month old lean and obese mice during 3 days of fasting and 2 days of refeeding, 6 weeks of dietary restriction, and 2 weeks of thyroxine (T4) administration. Obese mice produced slightly more total heat per animal at this age but weighed 1.5 to 2 times as much as lean mice and consumed more diet ad libitum. Heat production of obese mice was not as responsive to fasting as that of lean mice. When fed equal amounts of diet, obese mice continued to produce at least as much total heat as lean mice. Heat production of obese mice was more sensitive to T4 administration when compared to that of lean mice and unlike the lean mice, T4-treated obese mice were unable to adjust food intake to maintain body weight during a T4-induced increase in thermogenesis. These data suggest that metabolic responses of obese mice to changes in energy intake or output do not occur as rapidly as those of lean mice.

Effects of different carbohydrate types on energy balance, fatty acid synthesis, and plasma insulin concentrations in adrenalectomized ob/ob mice were investigated. Obese (ob/ob) and lean mice adrenalectomized at 4 wk of age received one of four high-carbohydrate powdered diets for 3 wk: stock, glucose, starch, or starch plus wheat bran. Adrenalectomy reduced energy intake of ob/ob mice equally independent of diet type, whereas energetic efficiency, in vivo rates of fatty acid synthesis in liver and white adipose tissue, and plasma insulin concentrations were substantially reduced to approach values in lean mice in all adrenalectomized ob/ob mice except those fed glucose. The ability of adrenalectomy to normalize energy balance in ob/ob mice depends on factors other than the reduced circulating concentration of glucocorticoids alone. Diet composition is a crucial factor, and striking differences exist between semipurified diets containing a simple sugar (glucose) and those containing a complex carbohydrate (starch), with no additional effect of dietary fiber (wheat bran).

Adult rats were fed diets containing 5 or 15% casein to determine effects of low protein intake on efficiency of energy retention and on brown adipose tissue metabolism. Efficiency of energy retention of rats fed the 5% casein diet for 4 or 8 weeks was approximately 40% lower than was efficiency of energy retention of rats fed the 15% casein diet. Rats fed the 5% casein diet also exhibited an enhanced norepinephrine (NE)-stimulated metabolic rate and an accelerated NE turnover in their brown adipose tissue relative to responses of rats fed the 15% casein diet. Additionally, NE turnover in white adipose tissue, but not heart, was accelerated in rats fed the 5% casein diet. The reduced efficiency of energy retention in rats fed the low protein diet may be linked to accelerated NE turnover and heat production by their brown adipose tissue.

[ 3 H]-Ouabain binding to muscle preparations was utilized to estimate the number of Na + ,K + -ATPase enzyme units in hindlimbs from 8 week old lean and obese mice. Specific [ 3 H]-ouabain binding per mg particulate protein was 36% lower in obese mice; whereas, the affinity of the binding sites for ouabain was similar in obese and lean mice. Since obese mice had less muscle than lean mice, the number of Na + ,K + -ATPase enzyme units in hindlimbs from obese mice was less than half the number observed in lean mice.

To determine if alterations in sympathetic nervous system (SNS) activity occur in rats with ventromedial hypothalamic (VMH) lesions, norepinephrine (NE) turnover rates were examined in various tissues of lesioned and control, weanling rats. VMH-lesioned rats fed a high-carbohydrate diet ad libitum for 4 weeks following surgery were not hyperphagic, but they gained 50% more body energy than control rats. VMH lesions extended the half-life of 3H-NE in interscapular brown adipose tissue (BAT) by 42%, in abdominal white adipose tissue (WAT) by 201%, in heart by 61% and in pancreas by 85%, and reduced total NE turnover (ng/organ/hr) in BAT (38%), WAT (57%), heart (30%) and pancreas (53%). Reduced SNS activity in BAT is consistent with the decreased energy expenditure (heat production) and increased energy efficiency observed in VMH-lesioned rats. In WAT, decreased SNS activity coupled with hyperinsulinemia would facilitate energy storage as fat by reducing lipid mobilization. In the pancreas, reduced SNS activity would contribute to hyperinsulinemia. These results support the hypothesis that VMH lesions decrease SNS activity in several organs. This change in autonomic tone is very likely a major factor in the development of obesity in VMH-lesioned animals.

SummaryThe number of Na+, K+-ATPase enzyme (EC 3.6.1.3) units in skeletal muscle and liver of 14-day-old lean and obese (ob/ob) mice was assayed from the concentration of high-affinity [3H]ouabain-binding sites in the tissue preparations. The number of [3H]ouabain-binding sites in forelimb and hindlimb muscles of obese mice was 28% lower than in lean littermates. In contrast, livers of lean and obese mice possessed equal numbers of [3H]ouabain-binding sites. The lower number of Na+,K+-ATPase enzyme units observed in skeletal muscle of the 14-day-old obese mice represents one of the earliest reported developmental alterations in an enzyme system in these mice and may be associated with the lower energy expenditure of young obese mice.

SummaryIn vivo rates of fatty acid synthesis in liver, removable adipose tissue, and mammary gland were obtained in mice. Liver contributed 60 to 65%, and adipose tissue 35 to 40% of the fatty acids synthesized in virgin mice fed a high-carbohydrate diet. Mice in the 18th and 19th day of gestation synthesized less than half the quantity of fatty acids synthesized in virgin mice, even though the pregnant mice consumed more food than the virgin mice. Rates of fatty acid synthesis were elevated more than threefold in lactating mice and 71 to 83% of the fatty acid synthesis occurred in the mammary gland of the lactating mice. Fasting for 12 hr or consumption of a high-fat diet for 5 days depressed rates of fatty acid synthesis in all three tissues examined. Removal of the pups for 12 hr decreased the rate of fatty acid synthesis in mammary gland and increased the rate in adipose tissue of lactating mice.

This study was undertaken to establish the time sequence of lipogenic changes in adipose tissue of rats when converted from ad libitum feeding to meal-eating. Rats were fed a high carbohydrate diet 2 hours/day for 0 to 10 days (meal-eating). The high speed supernatant fraction from homogenized epididymal fat pads was assayed for citrate cleavage enzyme, acetyl CoA carboxylase, fatty acid synthetase and malic enzyme activities. The effects of meal-feeding on in vitro and in vivo rates of fatty acid synthesis in adipose tissue as well as the amounts of glycogen deposited in the adipose tissue were measured. During the first 10 days of meal-feeding, the lipogenic enzyme activities were actually decreased or unchanged in the meal-fed rats but during this time the in vitro and in vivo rates of fatty acid synthesis were progressively increased in the meal-fed rats. Glycogen levels in the adipose tissue of meal-fed rats were greater than the levels in the nibblers. The initial hyperlipogenesis observed in the meal-fed rat appears to be due to changes in substrate uptake by the adipose tissue and/or to alterations in enzyme activation in the adipose tissue rather than to changes in the quantity of enzyme present in the tissue.

The hyperphagia and rapid body weight gain normally observed in young obese (ob/ob) mice were abolished by removal of their adrenal glands, whereas food intake and weight gain of lean mice were not significantly affected by adrenalectomy. Adrenalectomy lowered body energy density (kcal/g carcass) in obese mice more than could be attributed to reduced food intake per se, suggesting that their energy expenditure was also increased. In control obese mice, low stimulation of brown adipose tissue by the sympathetic nervous system, as indicated by the low fractional rates of norepinephrine (NE) turnover in their brown adipose tissue may have contributed to the reduced energy expenditure in these animals. Adrenalectomy increased the rates of NE turnover in brown adipose tissue of obese mice to rates nearly equal to those observed in lean mice without affecting NE turnover in this tissue of lean mice. Likewise, removal of the adrenals normalized the low rates of NE turnover in hearts of obese mice without affecting lean mice. Rates of NE turnover in two other organs, white adipose tissue and pancreas, of control and adrenalectomized obese mice were similar to rates observed in lean counterparts. The adrenal may thus contribute to both the hyperphagia and the low energy expenditure by brown adipose tissue that together cause gross obesity in ob/ob mice.

1. 1. Chickens weighing approx. 1500g were fasted 64 hr and then continuously infused with [6-3H]glucose to determine effects of ethanol on plasma glucose concentrations and on rates of glucose turnover. 2. 2. Ethanol infusions (222 or 444μmol/min × kg−1 body weight) did not cause hypoglycemia although the high dose infusion slightly decreased the rate of glucose turnover. 3. 3. Metabolite ratios measured in livers of chickens infused with the high dose of ethanol indicated that the hepatic cytosolic redox state was relatively unchanged. 4. 4. Chickens have an unusual resistance to ethanol-induced hypoglycemia.

Adrenalectomy arrests the development of obesity in ob/ob mice fed nonpurified high-starch diets partly by stimulating the low thermogenic activity of brown adipose tissue (BAT). However, adrenalectomy fails to suppress the development of obesity in ob/ob mice fed a purified high-glucose diet. Effects of adrenalectomy on BAT metabolism in ob/ob mice fed purified high-starch or high-glucose diets were therefore examined. Adrenalectomy markedly decreased the efficiency of energy retention and increased BAT metabolism (as assessed by GDP binding to BAT mitochondria, GDP-inhibitable acetate- or chloride-induced mitochondrial swelling, and by rates of norepinephrine turnover in BAT) in ob/ob mice fed a high-starch purified diet but had only minimal effects on energy efficiency or BAT metabolism in ob/ob mice fed a high-glucose purified diet. Plasma insulin concentrations decreased and thyroxine concentrations increased in adrenalectomized ob/ob mice fed the high-starch diet; changes in these hormones were less pronounced in adrenalectomized ob/ob mice fed the high-glucose diet. Consumption of glucose mimics effects of adrenal secretions on BAT metabolism in ob/ob mice.

1. 1. Chicks were fasted for 2 days and then refed a fat-free, a tripalmitin or a safflower oil containing diet for 5 days. 2. 2. Addition of safflower oil to the diet significantly depressed in vitro hepatic fatty acid synthesis and lipogenic enzyme activity. 3. 3. Tripalmitin was much less effective than safflower oil in depressing hepatic fatty acid synthesis. 4. 4. Both tripalmitin and safflower oil increased the rate of hepatic cholesterol synthesis. 5. 5. Since less than half of the dietary tripalmitin was absorbed, this may have been a major factor in the reduced response of the chick to this dietary lipid.

Six semipurified canned diets ranging in composition from 0 to 62% of energy from carbohydrate and from 20% to 48% of energy from protein were fed to female beagle dogs for 8 months. Additionally, three commercial-type diets were also fed. The effects of these diets on growth, body composition and selected blood metabolite levels in the dogs were studied. The dogs readily consumed each of the nine diets fed. The level of carbohydrate, fat or protein in the diet did not influence body weight gain during the first 16 weeks nor was nitrogen balance affected by the diets. At the end of the 32-week study, dogs fed the high-carbohydrate (62% of energy) diet contained less body fat but an equal-free mass, than did dogs fed lower-carbohydrate (20--42% of energy) diets with a similar quantity of protein. Consumption of carbohydrate-free diets did not influence postprandial levels of circulating glucose or insulin in the dogs. Plasma cholesterol levels were elevated in dogs consuming in the diets high in fat but plasma triglyceride levels were not influenced by the diets fed. Consumption of high-protein (46--48% of energy) diets elevated plasma urea nitrogen levels but had minimal influence on plasma amino acid levels. The general response of these young dogs was not markedly influenced by consumption of diets ranging from carbohydrate-free to high-carbohydrate and from adequate-protein to high-protein.

Rats fed low protein diets often exhibit an elevation in adaptive thermogenesis that may result in part from activation of thyroid hormone action at the level of peripheral deiodination of thyroxine (T4) to 3,5,3'-triiodothyronine (T3). This possibility was examined by comparing the kinetic parameters of iodothyronine 5'-deiodination in hepatic and renal microsomes and the efficiency of energy retention in weanling rats fed diets containing 5% (LP-5), 8% (LP-8) or 22% (NP) casein. Energy balance measurements revealed that efficiency of energy retention was reduced in rats fed LP-5, whereas no significant change in adaptive thermogenesis was observed in rats fed LP-8. In the LP-5 group the maximal activity of hepatic 5'-deiodinase per milligram of microsomal protein was not different from that of the NP group; however, the Vmax of the renal enzyme was 21% higher. In both tissues, the Km of the reaction was not affected by dietary treatment. Hepatic and renal 5'-deiodination in rats fed LP-8 was similar to that in rats fed LP-5. When compared to corresponding NP controls, each of the low protein dietary groups (LP-5, LP-8) had a higher serum total T3 concentration, whereas serum free T3 and total T4 concentrations were unaffected by the dietary treatments. The findings demonstrate that iodothyronine 5'-deiodination and circulating thyroid hormone concentrations vary in a similar manner in LP-5 and LP-8 animals even though these two groups exhibit different responses in energy efficiency relative to NP controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Female obese (ob/ob) and lean mice were weaned at 21 days of age, placed in wire-mesh cages maintained at 25 to 30 degrees, and fed a high-fat or a high-carbohydrate diet for 21 days. The body energy balance procedure was utilized to determine the maintenance energy requirements, and the efficiency of dietary energy utilization, above maintenance, in these mice. Heat production of each mouse was measured weekly in a gradient-layer calorimeter. Regressions of changes in body energy per kg3/4 on metabolizable energy intake per kg3/4 indicated that the maintenance energy requirement averaged 72 kcal/kg3/4/day for obese mice and 124 kcal/kg3/4/day for lean mice. Diet composition did not influence the maintenance energy requirements, but utilization of energy, above maintenance, in obese mice fed the high-fat diet was 41% more efficient than observed in obese mice fed the high-carbohydrate diet and 38 to 71% more efficient than observed in lean mice. Heat production, per unit body weight was lower in obese mice than in lean mice. The lowest heat production was observed in obese mice fed the high-fat diet. The 40% lower maintenance energy requirement of the obese mice is a major factor contributing to the high efficiency of energy retention in these mice. Consumption of a high-fat diet further improved the ability of the obese mice to retain dietary energy.

The influence of (-)-hydroxycitrate on in vitro rates of fatty acid synthesis in chicken and rat liver and in rat adipose tissue was investigated. Following acute and chronic administration of (-)-hydroxycitrate to chickens and rats, changes in rates of fatty acid synthesis in vivo and in lipogenic enzyme activities were also determined. Addition of 1 mM (-)-hydroxycitrate to a buffer containing 10 mM glucose and liver slices from chickens or rats depressed the rate of 3H2O incorporation into fatty acids. Acute administration of (-)-hydroxycitrate to chickens and rats also depressed in vivo rates of fatty acid synthesis in the livers of these species. Chickens appeared to be more sensitive to the inhibitory effects of (-)-hydroxycitrate than did rats. (-)-Hydroxycitrate was incorporated into the diets fed to the chickens and rats. Hepatic citrate cleavage enzyme activities were increased several fold in livers of chickens and rats fed (-)-hydroxycitrate. However, the rates of fatty acid synthesis in chicken and rat livers were depressed when expressed per g liver. Livers of chickens fed (-)-hydroxycitrate for 14 days were enlarged. Dietary (-)-hydroxycitrate did not depress rates of fatty acid synthesis per liver in these birds. Consumption of (-)-hydroxycitrate did not alter liver weight in rats. In vivo rates of fatty acid synthesis in rat adipose tissue were not influenced by consumption of a diet containing 52.6 nmoles (-)-hydroxycitrate/kg diet. Plasma triglyceride levels were increased two-fold in chickens, but unchanged in rats, fed (-)-hydroxycitrate for 2 to 3 weeks. There are species-specific as well as organ-specific responses to (-)-hydroxycitrate.

SummaryTwo lines of mice (O10 and C10) were derived from an ICR strain. The O10 mice weighed 52 g and contained 15.5% fat while the C10 mice weighed 36 g and contained 8.3% fat at 14 weeks of age. At this time, the O10 mice exhibited hyperglycemia and an increased rate of hepatic fatty acid synthesis when compared with the C10 mice. Although three other lines of mice (H6, C2, and L6) derived by reciprocally crossing CAF1 and AKD2F1 mice exhibited marked differences in body weight at 14 weeks of age (H6 = 37 g; C2 = 29 g; and L = 22 g), the percentage of body fat, blood glucose values, and in vitro rates of fatty acid synthesis in liver and adipose tissue were similar in these mice.

Publisher Summary This chapter discusses the effect of diet on activity of enzymes involved in fatty acid and cholesterol synthesis. Adipose tissue is the major organ contributing to de novo fatty acid synthesis in the nonlactating pig and ruminant, while the liver is more important in birds and man. In rats and mice, both organs contribute significantly to de novo fatty acid synthesis. In species such as the rat, where both liver and adipose tissue contribute to de novo fatty acid synthesis, dietary manipulations generally affect both tissues in a similar fashion; however, there are exceptions. The quantity of hepatic fatty acid synthetase can regulate the rate of fatty acid synthesis in rats fed high-carbohydrate diets. Unlike enzymes involved in fatty acid synthesis, a change in β -Hydroxy- β -methylglutaryl-CoA reductase activity precedes changes in hepatic acetate conversion to cholesterol. Allosteric control of enzyme activity plays a major role in the rapid regulation of metabolic flux. Adaptive changes in enzyme content reflect sustained changes in metabolic flux and such adaptations are involved in the longer term regulation of metabolism.

SummaryGlucose-U-14C conversion into triglycerides (in the presence of insulin) decreased as rat fat cells enlarged (and/or aged). The results of this study show that the diminished lipogenic capacity results from the marked decrease in glyceride-fatty acid biosynthesis while glucose conversion into glyceride-glycerol was unaltered by fat cell size.The authors thank Diane Dowd for her excellent technical assistance.

The possible involvement of Na+,K+-ATPase in the etiology of obesity in the obese (ob/ob) mouse was explored. The number of Na+,K+-ATPase enzyme units in skeletal muscle, liver, and kidneys from 4- and 8-wk-old obese and lean mice was estimated from saturable [3H]ouabain binding to particulate fractions. Neither phenotype nor age altered the Kd value for ouabain binding in these three tissue preparations. The total number of [3H]ouabain binding sites in hindlimb muscles was 35--55% lower in 4- and 8-wk-old obese mice than in their lean counterparts. However, the total number of [3H]ouabain binding sites in liver and kidneys of obese mice was similar to values observed in their lean counterparts. Because it has been suggested that ob/ob mice are hypothyroid, we investigated the response of Na+,K+-ATPase in these mice to thyroid hormone treatment (approximately 5 microgram thyroxine/day for 2 wk). The number of [3H]ouabain binding sites in the three tissues increased in both obese and lean mice injected with this relatively large dose of thyroxine, but the obese mice were 2--3 times more responsive than lean mice.

The effects of contrasting (16L:8D vs. 8L:16D) photoperiods on fat accretion and growth in 19 white-tailed doe fawns (Odocoileus virginianus) from 9 September to 16 December 1981 were examined. Fawns exposed to long days (LD fawns) delayed their autumn pelage change, whereas those exposed to short days (SD fawns) underwent a normal molt. SD fawns were heavier and accumulated more fat than their LD counterparts. The combined skeletal muscle and viscera of fawns exposed to short daylength contained 1,195 and 2,269 g of fat on 10 November and 16 December, respectively, as compared with 290 and 621 g of fat for LD fawns. SD fawns also had a higher daily intake of feed and were more efficient in converting dietary gross energy into tissue gross energy than LD fawns. Serum prolactin concentrations were substantially lower in SD fawns. Diminishing daylength appears to set the time frame for physiological events associated with fat accretion in white-tailed deer. J. WILDL. MANAGE. 48(3):776-787 Recently, researchers have become interested in evaluating the effects of photoperiod on certain physiological changes that deer undergo annually. Seasonal changes in pelage and feed intake have been linked to changing daylength in red deer (Cervus elaphus) (Pollock 1974, Kay and Ryder 1978). White-tailed deer, responding to an artificially extended summer photoperiod, delayed pelage change, and a decrease from a long day (16L:8D) to a short day (8L:16D) stimulated increased weight gain and sexual maturity (Budde 1983). Antler growth cycles also appeared to be mediated by photoperiod (Goss 1980). It is not clear how photoperiod induces these effects. Many physiological events are under hormonal control. The pineal gland, a light-sensitive organ, may play a role in mediating various hormone concentrations seasonally, thereby implicating changing daylength in circannual endocrine rhythms (Schulte et al. 1981). In domestic ruminants, serum prolactin concentrations follow a seasonal pattern, with lowest concentrations occurring during winter and highest concentrations during summer (Koprowski and Tucker 1973, Tucker et al. 1974). Similar seasonal patterns in prolactin concentrations have been demonstrated in white-tailed deer (Mirarchi et al. 1978, Schulte et al. 1980). Verme and Ozoga (1980) postulated that lipogenesis is mediated by a decline in prolactin and a rise in adrenocorticotrophic hormone, thereby suggesting a possible relationship between decreasing daylength (autumn), decreasing prolactin concentrations, and increased lipogenesis. The objective of this study was to determine the influence of different photoperiods on the growth and fat metabolism of white-tailed doe fawns as measured by 'Present address: Caesar Kleberg Wildlife Research Institute, Texas A&I University, Kingsville, TX 78363. 776 J. Wildl. Manage. 48(3):1984 This content downloaded from 157.55.39.132 on Thu, 15 Sep 2016 06:06:09 UTC All use subject to http://about.jstor.org/terms EFFECT OF PHOTOPERIOD ON DEER * Abbott et al. 777 changes in body composition and in vitro rates of fatty acid synthesis and lipolysis in adipose tissue. We appreciate the assistance provided by C. L. Bennett, W. S. Budde, T. M. Cooley, P. D. Friedrich, T. F. Reis, and L. L. Swanson of the Michigan Dep. of Nat. Resour. and by M. H. Clapsaddle, M. K. Hodge, G. C. Holt, W. V. Rumpler, G. C. Shurson, J. F. Sikarskie, P. A. Whetter, and J. R. Witwer of Michigan State Univ. This is Michigan Agric. Exp. Stn. J. Article 10797. The study was supported in part by the Michigan Dep. of Nat. Resour. through Federal Aid in Wildl. Restoration Proj. W-117-R.