Role of Choline Deficiency in the Fatty Liver?Phenotype of Mice Fed a Low Protein,Very Low Carbohydrate Ketogenic Diet

Though widely employed for clinical intervention in obesity, metabolic syndrome, seizure disorders and other neurodegenerative diseases, the mechanisms through which low carbohydrate ketogenic diets exert their ameliorative effects still remain to be elucidated. Rodent models have been used to identify the metabolic and physiologic alterations provoked by ketogenic diets. A commonly used rodent ketogenic diet (Bio-Serv F3666) that is very high in fat (~94% kcal), very low in carbohydrate (~1% kcal), low in protein (~5% kcal), and choline restricted (~300 mg/kg) provokes robust ketosis and weight loss in mice, but through unknown mechanisms, also causes significant hepatic steatosis, inflammation, and cellular injury. To understand the independent and synergistic roles of protein restriction and choline deficiency on the pleiotropic effects of rodent ketogenic diets, we studied four custom diets that differ only in protein (5% kcal vs. 10% kcal) and choline contents (300 mg/kg vs. 5 g/kg). C57BL/6J mice maintained on the two 5% kcal protein diets induced the most significant ketoses, which was only partially diminished by choline replacement. Choline restriction in the setting of 10% kcal protein also caused moderate ketosis and hepatic fat accumulation, which were again attenuated when choline was replete. Key effects of the 5% kcal protein diet – weight loss, hepatic fat accumulation, and mitochondrial ultrastructural disarray and bioenergetic dysfunction – were mitigated by choline repletion. These studies indicate that synergistic effects of protein restriction and choline deficiency influence integrated metabolism and hepatic pathology in mice when nutritional fat content is very high, and support the consideration of dietary choline content in ketogenic diet studies in rodents to limit hepatic mitochondrial dysfunction and fat accumulation.     

Photoperiod regulates dietary preferences and energy metabolism in young developing Fischer 344 rats but not in same-age Wistar rats

The effects of photoperiod on dietary preference were examined using young growing Fischer 344 and Wistar rats, which are seasonal and nonseasonal breeders, respectively. Rats were provided a low-fat, high-carbohydrate diet (LFD: 66/10/24% energy as carbohydrate/fat/protein) and high-fat, low-carbohydrate diet (HFD: 21/55/24% energy as carbohydrate/fat/protein) simultaneously under long- (LD: 16 h light/day) and short-day (SD: 8 h light/day) conditions for 3 wk. Fischer 344 rats preferred the LFD to the HFD under the LD condition, whereas preference for both diets was equivalent under the SD condition. Consequently, their body weight and total energy intake exhibited 11-15 and 10-13% increases, respectively, under the LD condition. Calculation of energy intake from macronutrients revealed that rats under the LD condition consumed 20-24 and 9-13% higher energy of carbohydrates and proteins, respectively, than those under the SD condition. In contrast, Wistar rats preferred the LFD to the HFD irrespective of photoperiod and exhibited no photoperiodic changes in any parameters examined. Next, Fischer 344 rats were provided either the LFD or HFD for 3 wk under LD or SD conditions. Calorie intake was 10% higher in the rats fed the LFD than those fed the HFD under SD condition. However, rats under LD condition exhibited 5-10, 14, and 64% increases in body weight, epididymal fat mass, and plasma leptin levels, respectively, compared with those under the SD condition irrespective of dietary composition. In conclusion, photoperiod regulates feeding and energy metabolism in young growing Fischer 344 rats via the interactions with dietary macronutrient composition.     

Effects of dietary fat content on adiposity during energy restriction in genetically obese rats.

The effects of the amount of fat provided in a restricted diet on weight loss and body composition were studied in this work. Lean male (Fa/?) Zucker rats were fed a control diet ad libitum. Obese (fa/fa) Zucker rats were divided into three groups: one group was fed a control diet ad libitum and the other two groups were fed 75% energy-restricted diets, which provided 10 or 50% of calories as fat. After 4 weeks, energy restriction normalized body weight but not body composition in the genetically obese rats. Reductions in adipose tissue weights and adipocyte size, without changes in the cellularity, were observed. Differences only reached statistical significance in subcutaneous adipose tissue. A standard fat content in the diet induced the same fat-free mass reduction as a higher amount of this macronutrient, but a greater body fat reduction. This suggests that the restriction of dietary fat, as well as energy, is necessary to achieve dietary management in obesity.     

A light- and electron-microscope study of hepatocytes of rats fed different diets

Ketogenic diets are used in the treatment of epilepsy in children refractory to drug therapy. This study identifies changes in liver morphology in rats fed four different diets: a normal rodent chow diet, a calorie-restricted high-fat (ketogenic) diet and each diet supplemented with clofibric acid. Hepatocytes of rats fed the ketogenic diet show many lipid droplets and these are reduced to control levels when clofibrate is present in the diet. Mitochondria are enlarged in the livers of rats fed the ketogenic diet and further enlarged if clofibrate is present. Alterations in the appearance or numbers of other organelles are also found.     

Influence of diet form on the hyperphagia-promoting effect of polysaccharide in rats

Adult female rats were fed chow only, or chow plus the polysaccharide Polycose presented as a solution (32% w/v), as a powder, or as a powder mixed into the chow diet. The rats fed the Polycose solution overate and gained three times as much weight as did the control rats in the 30-day test period. The rats fed the Polycose powder or mixed diet, on the other hand, did not differ from controls in food intake or weight gain. The solution-fed rats consumed more Polycose than did the powder-fed rats, but the two groups were equivalent in their chow intake. The absolute and percent body fat of the solution-fed rats exceeded that of control rats, as well as that of powder and mixed-diet animals. The percent body fat of the powder and mixed diet groups exceeded that of the control animals. The findings demonstrate that the form of diet presentation has a major impact on the rat's feeding and body weight responses to polysaccharide diets.     

Dietary modulation of circulating leptin levels: site-specific changes in fat deposition and ob mRNA expression.

In order to study the effects of diet on fat distribution, circulating leptin levels and ob mRNA expression, diets of different macronutrient composition were fed to lean mice and gold thioglucose-obese mice. A high-fat diet and 2 high-carbohydrate diets, one containing mostly high-glycaemic-index starch and the other containing low-glycaemic-index starch were fed ad libitum for 10 weeks and were compared to standard laboratory chow. Weight gain was attenuated by feeding low-glycaemic-index starch in all mice and by feeding a high-fat diet in lean mice. Reduced adiposity was seen in lean mice fed low-glycaemic-index starch, whereas increased adiposity was seen in both lean and obese mice fed on the high-fat diet. Circulating leptin levels, when corrected for adiposity, were decreased in all mice fed either the high-fat diet or the low-GI diet. In epididymal fat pads, decreased ob mRNA expression was seen after both high-fat and high-glycaemic-index starch feeding. These results show that diet macronutrient composition contributes to the variability of circulating leptin levels by the combined effects of diet on fat distribution and on site-specific changes in ob mRNA expression.     

Effects of fructose and glucose on plasma leptin, insulin, and insulin resistance in lean and VMH-lesioned obese rats

To determine the influence of dietary fructose and glucose on circulating leptin levels in lean and obese rats, plasma leptin concentrations were measured in ventromedial hypothalamic (VMH)-lesioned obese and sham-operated lean rats fed either normal chow or fructose- or glucose-enriched diets (60% by calories) for 2 wk. Insulin resistance was evaluated by the steady-state plasma glucose method and intravenous glucose tolerance test. In lean rats, glucose-enriched diet significantly increased plasma leptin with enlarged parametrial fat pad, whereas neither leptin nor fat-pad weight was altered by fructose. Two weeks after the lesions, the rats fed normal chow had marked greater body weight gain, enlarged fat pads, and higher insulin and leptin compared with sham-operated rats. Despite a marked adiposity and hyperinsulinemia, insulin resistance was not increased in VMH-lesioned rats. Fructose brought about substantial insulin resistance and hyperinsulinemia in both lean and obese rats, whereas glucose led to rather enhanced insulin sensitivity. Leptin, body weight, and fat pad were not significantly altered by either fructose or glucose in the obese rats. These results suggest that dietary glucose stimulates leptin production by increasing adipose tissue or stimulating glucose metabolism in lean rats. Hyperleptinemia in VMH-lesioned rats is associated with both increased adiposity and hyperinsulinemia but not with insulin resistance. Dietary fructose does not alter leptin levels, although this sugar brings about hyperinsulinemia and insulin resistance, suggesting that hyperinsulinemia compensated for insulin resistance does not stimulate leptin production.     

Reduced central leptin sensitivity in rats with diet-induced obesity

On low-fat chow diet, rats prone to diet-induced obesity (DIO) have increased arcuate nucleus neuropeptide Y (NPY) expression but similar leptin levels compared with diet-resistant (DR) rats (19). Here, body weight and leptin levels rose in DIO rats, and they defended their higher body weight after only 1 wk on a 31% fat high-energy (HE) diet. However, DIO NPY expression did not fall to DR levels until 4 wk when plasma leptin was 168% of DR levels. When switched to chow, DIO rats lost carcass fat (18). By 10 wk, leptin levels fell to 148% and NPY expression again rose to 150% of DR levels. During 4 wk of food restriction, DIO leptin fell by approximately 50% while NPY increased by 30%. While both returned to control levels by 8 wk, DIO rats still regained all lost weight when fed ad libitum. Finally, the anorexic effect of intracerebroventricular leptin (10 microg) was inversely correlated with subsequent 3-wk weight gain on HE diet. Thus NPY expression and food intake are less sensitive to the leptin's suppressive effects in DIO rats. While this may predispose them to develop DIO, it does not fully explain their defense of a higher body weight on HE diet.     

Three weeks of early-onset exercise prolongs obesity resistance in DIO rats after exercise cessation

We assessed the effect of early-onset exercise as a means of preventing childhood obesity using juvenile male rats selectively bred to develop diet-induced obesity (DIO) or to be diet resistant (DR) when fed a 31% fat high-energy diet. Voluntary wheel running begun at 36 days of age selectively reduced adiposity in DIO vs. DR rats. Other 4-wk-old DIO rats fed a high-energy diet and exercised (Ex) for 13 wk increased their core temperature, gained 22% less body weight, and had 39% lighter fat pads compared with sedentary (Sed) rats. When wheels were removed after 6 wk (6 wk Ex/7 wk Sed), rats gained less body weight over the next 7 wk than Sed rats and still had comparable adipose pad weights to 13-wk-exercised rats. In fact, only 3 wk of exercise sufficed to prevent obesity for 10 wk after wheel removal. Terminally, the 6-wk-Ex/7-wk-Sed rats had a 55% increase in arcuate nucleus proopiomelanocortin mRNA expression vs. Sed rats, suggesting that this contributed to their sustained obesity resistance. Finally, when Sed rats were calorically restricted for 6 wk to weight match them to Ex rats (6 wk Rstr/7 wk Al), they increased their intake and body weight when fed ad libitum and, after 7 wk more, had higher leptin levels and adiposity than Sed rats. Thus, early-onset exercise may favorably alter, while early caloric restriction may unfavorably influence, the development of the hypothalamic pathways controlling energy homeostasis during brain development.     

Comparison of Fat Storage between Fischer 344 and Obesity‐Resistant Lou/C Rats Fed Different Diets**

Objective: We aimed to characterize further the Lou/C (LOU) and Fischer 344 (F344) rat strains for nutritional traits to validate their use as contrasting strains for molecular genetic studies. Research Methods and Procedures: Five batches of LOU and F344 rats were used to measure caloric intake, weight gain, and body composition when fed a chow diet, a self‐selection diet (together with the study of preferences for macronutrients), hypercaloric diets, and a chow diet in a cold environment. Results: Despite a higher caloric intake when fed a chow diet, LOU rats showed a lower weight gain, final body weight, and percentage of fat tissue, together with a higher percentage of carcass weight, than F344 rats. When fed a self‐selection diet, LOU males ingested less protein and more fat than F344 males, and the reverse was observed for females. In this condition, feed efficiency was reduced in LOU but increased in F344 rats compared with the chow diet. Diet‐induced obesity was observed in F344 rats but not in LOU rats fed hypercaloric diets. In a cold environment, both LOU and F344 rats displayed an increased percentage of brown adipose tissue compared with control groups, together with a higher caloric intake. Discussion: The study shows robust nutritional differences between the LOU rat, a lean strain with a low feed efficiency and resistant to diet‐induced obesity, and the contrasting F344 rat strain. It also shows the interest in these strains for studying the genetic components of resistance to obesity.     

Short-term, increasing dietary protein and fat moderately affect energy expenditure, substrate oxidation and uncoupling protein gene expression in rats

Macronutrient composition of diets can influence body-weight development and energy balance. We studied the short-term effects of high-protein (HP) and/or high-fat (HF) diets on energy expenditure (EE) and uncoupling protein (UCP1-3) gene expression. Adult male rats were fed ad libitum with diets containing different protein-fat ratios: adequate protein-normal fat (AP-NF): 20% casein, 5% fat; adequate protein-high fat (AP-HF): 20% casein, 17% fat; high protein-normal fat (HP-NF): 60% casein, 5% fat; high protein-high fat (HP-HF): 60% casein, 17% fat. Wheat starch was used for adjustment of energy content. After 4 days, overnight EE and oxygen consumption, as measured by indirect calorimetry, were higher and body-weight gain was lower in rats fed with HP diets as compared with rats fed diets with adequate protein content (P<.05). Exchanging carbohydrates by protein increased fat oxidation in HF diet fed groups. The UCP1 mRNA expression in brown adipose tissue was not significantly different in HP diet fed groups as compared with AP diet fed groups. Expression of different homologues of UCPs positively correlated with nighttime oxygen consumption and EE. Moreover, dietary protein and fat distinctly influenced liver UCP2 and skeletal muscle UCP3 mRNA expressions. These findings demonstrated that a 4-day ad libitum high dietary protein exposure influences energy balance in rats. A function of UCPs in energy balance and dissipating food energy was suggested. Future experiments are focused on the regulation of UCP gene expression by dietary protein, which could be important for body-weight management.     

Dietary supplementation with Pluronic L-81 modifies hepatic secretion of very low density lipoproteins in the rat

Supplementation of high fat/cholesterol-enriched diets with polyoxypropylene-polyoxyethylene copolymers containing 90% hydrophobic constituents has been found to impair enteric secretion of chylomicrons, lower plasma levels of very low density (VLDL) and low density (LDL) lipoprotein cholesterol and prevent diet-induced hypercholesterolemia and atherosclerosis. These agents are known to be absorbed from the gastrointestinal tract and excreted in bile. In order to determine whether dietary supplementation with this group of hydrophobic poloxalenes influences hepatic secretion of triglyceride-rich lipoproteins, groups of rats were maintained for 21-34 days on either standard chow, semisynthetic diet containing 10.0% safflower oil/1.0% cholesterol, or each of the above diets supplemented with the hydrophobic poloxalene Pluronic L-81. At the end of the feeding period, newly secreted hepatic VLDL were isolated from 2-hr recirculating liver perfusates, quantitated, and characterized. Compared to perfusions in chow-fed rats, perfusion experiments in rats fed the high fat/cholesterol-enriched semisynthetic diet revealed a 3.1-fold increased net hepatic VLDL secretion rate; enrichment of secretory VLDL in cholesteryl esters and in C18:2 core lipid fatty acids; and a shift in the size distribution of secretory VLDL towards larger particles. When the 0.5% Pluronic L-81 was included in the high fat/cholesterol-enriched semisynthetic diet, the net hepatic VLDL secretion rate fell significantly and the physicochemical properties of secretory VLDL in these rats were found to resemble those of chow-fed animals. Supplementation of the chow diet with L-81 resulted in a significant fall in the net hepatic VLDL secretion rate from that observed in rats fed chow alone. Compared to rats fed chow alone, perfusate VLDL from rats fed each of the other experimental diets contained markedly lower amounts of both apoB molecular weight variants, as analyzed by gradient gel electrophoresis and densitometric gel scanning. Since previous studies have demonstrated that VLDL are the major cholesterol transport lipoproteins following fat/cholesterol feeding; a precursor-product relationship exists between fat/cholesterol-induced hepatic VLDL and plasma VLDL; such particles are capable of delivering cholesterol to the arterial wall; and dietary supplementation with hydrophobic poloxalenes prevents both the increase in plasma VLDL-cholesterol and diet-induced atherosclerosis, it is possible that dietary supplementation with hydrophobic poloxalenes may influence the atherogenic process through direct and/or indirect effects on hepatic VLDL transport.     

Feeding Response of Rats to No-Fat and High-Fat Cakes

The nutritional effects of high-fat diets have been extensively studied in laboratory animals, but as yet few experiments have examined the feeding response of animals to newly developed fat substitutes. The present study used commercially available no-fat (0% fat, 92% carbohydrate) and high-fat (41% fat, 54% carbohydrate) cake to determine the effects of fat substitutes on food preference and caloric intake in rats. The first experiment showed that nondeprived rats found the high-fat and no-fat cakes equally palatable and highly preferred to lab chow. Food deprived rats, however, preferred the high-fat cake to the no-fat cake, which may be related to its higher caloric density. In the second experiment, rats fed high-fat cake, in addition to chow, for 30 days consumed more calories and gained more weight than did rats fed no-fat cake and chow. The no-fat cake group, however, overate and gained more weight than chow-only controls. The hyperphagic response to the no-fat cake can be attributed to its carbohydrate content, moisture, and high palatability. Thus, removing fat from the cake reduced, but did not eliminate, its obesity-promoting effect. Obviously, low-fat foods must be consumed in moderation if used for weight control.     

高脂喂养合并小剂量链脲佐菌素建立2型糖尿病大鼠模型

目的 观察不同配方的高脂饲料,以及不同周龄的大鼠对于该模型的造模成功率和模型病变特点的影响.方法 将26只3周龄SD大鼠分为正常一组(N1组)、模型一组(M1组)和模型二组(M2组);26只5周龄SD大鼠分为正常二组(N2组)、模型三组(M3组)和模型四组(M4组).M1组和M3组给予高脂饲料配方一喂养,M2组和M4组给予高脂饲料配方二喂养.4周后,各模型组大鼠腹腔注射STZ溶液35 mg/kg.连续观察大鼠的空腹血糖(FBG)、空腹胰岛素(FIN)、总胆固醇(TG)、甘油三酯(TC)水平.结果 5周龄SD大鼠的FBG水平在注射STZ后两周即可达到稳定状态,并维持在较高的水平;高脂饲料配方二使大鼠的进食量和体重增加明显,并且成功诱导出胰岛素抵抗( insulin resistance,IR).结论 选取5周龄SD大鼠作为模型动物,并给予配方二高脂饲料喂养,所建立的大鼠模型具备2型糖尿病的主要特征,是值得推广的2型糖尿病动物模型.     

L-阿拉伯糖对降低高糖高脂喂养小鼠体重增长速率的影响

将L-阿拉伯糖通过口服的方法配合高糖高脂饲料喂养SPF级昆明雄性小鼠,观察不同剂量L-阿拉伯糖对小鼠增重速率的影响。将100只小鼠随机均分为A、B、C、D、E五组(五组小鼠体重没有显著差异),分别采用高、中、低和零四种剂量水平口服L-阿拉伯糖水溶液1个月,另设E组为空白对照,记录小鼠体重和体长变化。结果表明:L-阿拉伯糖对小鼠的体重增长有剂量依存关系,小剂量(0.5g/kg)即可产生作用,但只有添加量达到一定的浓度后(1.0g/kg),其抑制小鼠体重增长速率作用才有明显效果(P0.05)。L-阿拉伯糖能有效减缓肥胖小鼠的体重增长速率。     

Lipoprotein lipase and lipogenic enzyme activities in adipose tissue from rats fed different lipid sources

This work was designed to study the effect of different lipid sources on the activities of lipoprotein lipase and lipogenic enzymes in adipose tissue from rats fedad libitum or energy-controlled diets. Male Wistar rats were fed diets containing 40% of energy as fat (olive oil, sunflower oil, palm oil or beef tallow), for 4 wk. Underad libitum feeding no differences were found among dietary fat groups in final body weight, adipose tissue weights and total body fat. Under energy-controlled feeding, despite isoenergetic intake, rats fed the beef tallow diet gained significantly less weight than rats fed the other three diets. Beef tallow fed rats showed the lowest values for adipose tissue weights and total body fat. When rats had free access to food no effect of dietary lipid source on lipogenic enzyme activities was found. In contrast, under energy-controlled feeding rats fed the beef tallow diet showed significantly higher activities of glucose-6-phosphate dehydrogenase and fatty acid synthase than rats fed the other three diets. Heparin-releasable lipoprotein lipase activity in perirenal and subcutaneous adipose tissues was not different among rats fed olive oil, safflower oil, palm oil or beef tallow. When comparing both adipose tissue anatomical locations, significantly higher activities were found in subcutaneous than in perirenal fat pad independently of dietary fat. In conclusion, under our experimental protocol, lipogenesis in rat adipose tissue does not seem to be affected by dietary fat type.     

Effect of dietary polyunsaturated fat and 7,12-dimethylbenz(a)-anthracene on rat splenic natural killer cells and prostaglandin E synthesis

Summary Dietary polyunsaturated fat has been shown to stimulate mammary tumorigenesis induced in rats by 7,12-dimethylbenz(a)anthracene (DMBA). Studies were undertaken to investigate the effect of polyunsaturated fat and DMBA on splenic natural killer (NK) activity and prostaglandin E (PGE) synthesis. In a first experiment, splenic NK activity at 33, 55, 75, and 110 days of age was measured in Sprague-Dawley rats fed 0.5% low fat (LF), 5% normal fat (NF), or 20% high fat (HF) corn oil diets from 23 days of age. At 55 days of age, half of the rats from the 75 and 110 day age groups were given 5 mg DMBA. Ten days after the initiation of the diets splenic NK activity against YAC-1 lymphoma was decreased from 50% cytotoxicity in rats fed NF diet to 21% cytotoxicity in rats fed HF diet, but was not affected by LF feeding. No difference in NK activity was observed among the groups at the later time periods. DMBA had no effect on NK activity at 20 or 55 days after its administration. In a second experiment, where DMBA (15 mg/rat) was given to half of the rats at 50 days of age and NF or HF diets were started 3 days later, NK activity was 35% in rats fed NF diet and 21% in rats fed HF diet, 5 days after the diets were started. No difference in NK activity in rats fed either diet was observed at later time periods. DMBA decreased both NK activity and spleen cellularity transiently. In both experiments, PGE synthesis by spleen cells cultured for 18 h was not affected by dietary fat intake, but was slightly increased 3 days after DMBA administration. Results from these experiments suggest that the stimulation of DMBA-induced mammary tumorigenesis by polyunsaturated fat and by DMBA itself may possibly be mediated by a transient decrease in splenic NK cell activity.This work was supported by grants CA-35641, CA-33240, CA-13038 and Core Grant CA-24538 from the National Cancer Institute     

Influence of dietary macronutrient composition on adiposity and cellularity of different fat depots in Wistar rats

The aim of this study was to investigate the role of dietary macronutrient content on adiposity parameters and adipocyte hypertrophy/hyperplasia in subcutaneous and visceral fat depots from Wistar rats using combined histological and computational approaches. For this purpose, male Wistar rats were distributed into 4 groups and were assigned to different nutritional interventions: Control group (chow diet); high-fat group, HF (60% E from fat); high-fat-sucrose group, HFS (45% E from fat and 17% from sucrose); and high-sucrose group, HS (42% E from sucrose). At day 35, rats were sacrificed, blood was collected, tissues were weighed and fragments of different fat depots were kept for histological analyses with the new softwareAdiposoft. Rats fed with HF, HFS and HS diets increased significantly body weight and total body fat against Control rats, being metabolic impairments more pronounced on HS rats than in the other groups. Cellularity analyses usingAdiposoft revealed that retroperitoneal adipose tissue is histologically different than mesenteric and subcutaneous ones, in relation to bigger adipocytes. The subcutaneous fat pad was the most sensitive to the diet, presenting adipocyte hypertrophy induced by HF diet and adipocyte hyperplasia induced by HS diet. The mesenteric fat pad had a similar but attenuated response in comparison to the subcutaneous adipose tissue, while retroperitoneal fat pad only presented adipocyte hyperplasia induced by the HS diet intake after 35 days of intervention. These findings provide new insights into the role of macronutrients in the development of hyperplastic obesity, which is characterized by the severity of the clinical features. Finally, a new tool for analyzing histological adipose samples is presented.     

Influence of diet and carnitine palmitoyltransferase I inhibition on myosin and sarcoplasmic reticulum.

To examine the role of metabolic signals for ventricular myosin expression and activity of the sarcoplasmic reticulum Ca2+ pump, Wistar rats were treated for 7-8 wk with 5 or 50 mg/kg etomoxir, which inhibits fatty acid utilization. The proportion of myosin V1 was increased (P less than 0.05) with 50 mg/kg etomoxir (75 +/- 5% vs. 62 +/- 6% of control rats), whereas both doses increased the rate of Ca2+ uptake. A carbohydrate-rich fat-free diet or 8% sucrose drinking solutions, however, had no effect on myosin and sarcoplasmic reticulum. When rats were fed diets with an increased content (10 or 20%) of sunflower oil, the calorie intake and myosin V1 increased (56 +/- 8 or 64 +/- 8% vs. 44 +/- 6% of control rats). Isocaloric 10% fat diets of varying fatty acid composition (coconut fat, olive oil, or mackerel oil) also induced a higher calorie intake and increased V1 (64 +/- 6, 60 +/- 9, or 65 +/- 8% for the respective oils vs. 44 +/- 6% of control rats) but did not significantly increase rate of Ca2+ uptake. We concluded that calorie-rich diets changed the myosin expression not by affecting the ratio of fatty acid to glucose utilization but via the increased calorie intake.