Hydrogenated fat intake during pregnancy and lactation modifies serum lipid profile and adipokine mRNA in 21-day-old rats

OBJECTIVE: We examined whether feeding pregnant and lactating rats hydrogenated fats rich in trans-fatty acids modifies the plasma lipid profiles and the expression of adipokines involved with insulin resistance and cardiovascular disease in their 21-d-old offspring. METHODS: Pregnant and lactating Wistar rats were fed with a control diet (C group) or one enriched with hydrogenated vegetable fat (T group). After delivery, male offspring were weighed weekly and killed at day 21 of life by decapitation. Blood and retroperitoneal, epididymal, and subcutaneous white adipose tissues were collected. RESULTS: Offspring of T-group rats had increased serum triacylglycerols and cholesterol, white adipose tissue plasminogen activator inhibitor-1, and tumor necrosis factor-alpha gene expression, and carcass lipid content and decreased blood leptin and adiponectin and adiponectin gene expression. CONCLUSION: Ingestion of hydrogenated vegetable fat by the mother during gestation and lactation alters the blood lipid profiles and the expression of proinflammatory adipokynes by the adipose tissue of offspring aged 21 d.     

Hydrogenated fat intake during pregnancy and lactation caused increase in TRAF-6 and reduced AdipoR1 in white adipose tissue,but not in muscle of 21 days old offspring rats

Background  

Although lipids transfer through placenta is very limited, modification in dietary fatty acids can lead to implications in fetal and postnatal development. Trans fatty acid (TFA) intake during gestation and lactation have been reported to promote dyslipidemia and increase in pro- inflammatory adipokines in offspring. The aim of this study was to evaluate whether the alterations on pro-inflammatory cytokines and dyslipidemia observed previously in 21-d-old offspring of rats fed a diet containing hydrogenated vegetable fat during gestation and lactation were related to alterations in TLR-4, TRAF-6 and adipo-R1 receptor in white adipose tissue and muscle. On the first day of gestation, rats were randomly divided into two groups: (C) received a control diet, and (T) received a diet enriched with hydrogenated vegetable fat, rich in trans fatty acids. The diets were maintained throughout gestation and lactation. Each mother was given eight male pups. On the 21st day of life the offspring were killed. Blood, soleus and extensor digital longus (EDL) muscles, and retroperitoneal (RET) white adipose tissue were collected.     

Effects of age, diet and lactation on lipogenesis in rat adipose, liver and mammary tissues

Four diets varying in safflower oil content from zero to 20% were used in a study of interactions among diet and physiological state. Increasing fat in the diet did not alter food intakes but decreased digestibility coefficients. Increasing safflower oil intake did not alter milk fat content in lactating rats but increased relative amounts of unsaturated fatty acids in milk fat. In liver and perirenal adipose tissues from young male and non-lactating female rats, low fat diets increased rates of lipogenesis from glucose in vitro and specific activities of enzymes whose functions are closely associated with lipogenesis. This adaptive hyperlipogenic response was not evident or was less prominent in aged or lactating rats. In the case of lactating rats it appears that lactation produces a marked reduction in adipose lipogenesis when low fat diets are fed. Reduced glyceride glycerol synthesis in lactating as compared to non-lactating rat adipose coupled with reduced fatty acid synthesis and in increased lipolysis indicated a shift in adipose function in the direction of increased fat mobilization as would be supportive of lactation. Only minor diet effects upon mammary enzyme patterns and rates of in vitro lipogenesis were observed.     

Linoleate enrichment of diet and prostaglandin metabolism in rats.

Evidence that biosynthesis of prostaglandins (PG) in tissues of animals deficient in essential fatty acids is dependent on the availability of their precursors has been demonstrated. The purpose of this study was to determine the following: (1) effects of dietary linoleate enrichment on PG biosynthesis in rats; (2) effects of exogenous PGE2 and dietary linoleate on plasma free fatty acids and serum cholesterol in fed and fasted rats. Rats were fed three different concentrations of dietary linoleate as beef tallow, hydrogenated vegetable fat, or corn oil. The concentrations of PGE1 and PGF2a measured by radioimmunoassay were higher in rats fed the fed the beef tallow diet independent of energy status. A decrease in the concentration of PG between fasted and fed rats receiving hydrogenated vegetable fat is discussed in respect to the possible influence of trans isomers of unsaturated fatty acids on the biosynthesis of PG. There were significant effects of fasting on serum cholesterol concentration regardless of diet and significant interactions among effects of PGE2, fasting, and diet, suggesting regulatory effects of PGE2 on serum cholesterol concentration. The increase in plasma free fatty acids associated with fasting was prevented by PGE2 for all diets, but had the most marked effect on rats fed hydrogenated vegetable fat.     

Trans fatty acids in maternal milk lead to cardiac insulin resistance in adult offspring

OBJECTIVE: Trans fatty acids (TFAs) are derived from vegetable oil hydrogenation and can be found in most manufactured food products. Our main objective was to evaluate the effects of TFA consumption by lactating dams on cardiac glucose metabolism of adult offspring by analyzing glucose transporter-4 in the left ventricle. To investigate the energy homeostasis, insulin sensitivity and hepatic glycogen content were also measured. METHODS: Lactating Wistar rats were divided into a control group or a TFA group. The control group received a diet containing soybean oil, and the TFA group received a diet containing partially hydrogenated vegetable oil (total trans concentration of about 10.58 mg/g, 11.75%, of total fat) throughout the lactation period. At weaning, pups from both groups received a standard chow until 60 d of age, at which time the quantity of glucose transporter-4 in the left ventricle and hepatic glycogen were measured. Moreover, insulin sensitivity was analyzed by assessing the insulin/glucose ratio and the homeostatic model assessment index. RESULTS: TFA consumption by the pups during lactation led to a significant decrease in the cardiac content of glucose transporter-4 (P < 0.05) and in the hepatic content of glycogen (P < 0.05). Moreover, we observed impaired insulin sensitivity in the TFA group (insulin/glucose ratio and homeostatic model assessment index, P < 0.05) in adulthood. CONCLUSION: Our data suggest that the consumption of hydrogenated fat, rich in TFAs, by the mothers during the lactation period caused cardiac insulin resistance in the adult progeny, thus reinforcing the hypothesis that early adaptations may cause deleterious consequences later in life.     

Changes in UCP family expressions in rat tissues due to diet and aging

Regulation of the gene expressions of uncoupling proteins (UCP)-1, 2 and 3 was investigated in the white and brown adipose tissues and skeletal muscle of young and old rats (8-wk- and 8-mo-old, respectively) fed diets containing various fats (hydrogenated fat, corn oil or fish oil) and proteins (casein or soybean) for 1 wk. The mRNA expressions of UCP-1, 2 and 3 were elevated in the white adipose tissues of the young rats fed soybean protein as compared to those fed casein, and that of UCP-2 was also elevated in the brown adipose tissue. The effects of dietary fat type on the expressions were not clear. The UCP-1, 2 and 3 mRNA expressions were markedly reduced in the tissues of the old rats. The UCP-2 expressions were more markedly elevated by dietary soybean protein and reduced by aging than the others, particularly in the white adipose tissue. The expressions of leptin involved in thermogenesis were also reduced by aging. Moreover, in a fasted-refed experiment conducted for the young rats, UCP-2 mRNA induction in the white adipose tissues reached maximal levels at 1 or 2 h and was stimulated by dietary fat or soybean protein. Thus, UCP-2 mRNA expression was markedly affected by diet and aging, particularly in white adipose tissue.     

Ethanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of beta-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.     

Maternal low-protein diet during lactation programmes body composition and glucose homeostasis in the adult rat offspring

Previously we have reported that maternal malnutrition during lactation programmes body weight and thyroid function in the adult offspring. In the present study we evaluated the effect of maternal protein restriction during lactation upon body composition and hormones related to glucose homeostasis in adult rats. During lactation, Wistar lactating rats and their pups were divided into two experimental groups: control (fed a normal diet; 23% protein) and protein-restricted (PR; fed a diet containing 8% protein). At weaning, offspring received a normal diet until they were 180 d old. Body weight (BW) and food intake were monitored. Serum, adrenal glands, visceral fat mass (VFM) and carcasses were collected. PR rats showed lower BW (-13%; P < 0.05), VFM (-33%; P < 0.05), total body fat (-33%; P < 0.05), serum glucose (-7%; P < 0.05), serum insulin (-26%, P < 0.05), homeostasis model assessment index (-20%), but higher total adrenal catecholamine content (+90%; P < 0.05) and serum corticosterone concentration (+51%; P < 0.05). No change was observed in food intake, protein mass or total body water. The lower BW of PR rats is due to a reduction of white fat tissue, probably caused by an increase in lipolysis or impairment of lipogenesis; both effects could be related to higher catecholaminergic status, as well as to hypoinsulinaemia. To conclude, changes in key hormones which control intermediary metabolism are programmed by maternal protein restriction during lactation, resulting in BW alterations in adult rats.     

Dietary supplementation increases milk output in the rat

The effects of dietary supplementation on milk output and maternal body composition were investigated in the lactating rat. The supplement was a cooked homogeneous mixture of eggs and maize oil, and had the same protein-energy: total energy value as the control diet. During 2-12 d post partum rats were fed ad lib., either on the control diet alone or on the control diet plus the supplement. Measurements were made of milk output using an isotope-dilution technique, milk composition, and dam and litter body-composition changes. Compared with the dams receiving only the control diet, dams provided with the supplement consumed 19.7% more energy and protein and produced 31.2% more milk and mobilized less body fat. By 12 d of age, pups in litters of dams receiving the supplement were significantly heavier than those in litters of dams receiving the control diet only, and they contained more protein and more fat. It is concluded that dietary supplementation of lactating rats can enhance lactational performance.     

Effect of food preservatives on mother rats and survival of their offspring

This work aimed to investigate the effect of food preservatives (sodium benzoate and sodium nitrite) on biochemical aspects of mother rats and survival of their offspring. Fifty pregnant albino rats (Sprague Dauley strain) were divided into 5 groups (10 rats each) and kept individually in wire cages. The first group was fed standard diet free from any additives (control group). The second and third groups were fed standard diet with added acceptable and high doses of sodium benzoate as a preservative. The fourth and fifth groups were fed on standard diet containing sodium nitrite at the same levels like that for benzoate in the second and the third groups. Animals were fed ad libitum during pregnancy. After delivery, the pups were measured anthropometrically (weight and length) and the mothers were sacrificed and their blood samples were taken from the hepatic portal vain. Serum was separated and subjected to biochemical analysis. The results indicated that sodium nitrite intake was associated with a significantly decreased food intake and lowered hemoglobin and hematocrit values (p<0.01 each) while their serum AST and ALP showed significantly higher values (p<0.01). Mothers receiving high dose of benzoate had significantly high ALT values (p<0.01). Both levels of benzoate and nitrite were shown to induce decrease in serum bilirubin and increased serum urea, while the high and acceptable doses of benzoate induced higher values of serum uric acid (p<0.01 and p<0.05, respectively), but did not induce a significant increase in serum creatinine. Pregnant rats which received acceptable and high doses of nitrite showed an increased mortality rate of their pups. The mean weight and length of live pups were lowered by food preservatives compared with controls.     

饮食诱导肥胖抵抗大鼠激素敏感脂肪酶基因的表达

目的　探讨高脂饮食诱导肥胖抵抗 (DIO R)大鼠激素敏感脂肪酶基因的表达。方法5 0只健康雄性SD大鼠 ,随机分为对照组和高脂组 ,分别用基础饲料和高脂饲料喂养 13周 ,然后根据体重和能量摄入量筛选出DIO R和饮食诱导肥胖 (DIO)组 ,观察体脂含量的变化 ,放免法测血清生长激素含量 ,RT PCR法测定大鼠激素敏感脂肪酶mRNA水平。结果　DIO R大鼠体脂含量为 (4 2 6±0 5 1) % ,低于DIO大鼠的 (5 34± 0 34) % ;DIO R大鼠血清生长激素水平为 (0 70± 0 0 6 )ng/ml,高于DIO大鼠的 (0 5 0± 0 0 8)ng/ml;高脂饲料可增加DIO R大鼠白色脂肪激素敏感脂肪酶mRNA水平。结论　大鼠白色脂肪中激素敏感脂肪酶表达增加在大鼠肥胖抵抗的发生中起一定作用。     

Effects of dietary protein, fat and restriction on body composition and energy balance in lactating rats

Isoenergetic diets formulated at three levels of dietary protein using 12,24 and 40% casein and at two levels of fat using 2.26 and 13.82% corn oil were fed at five levels of intake, ad libitum, 75, 62.5, 50 and 37.5% of average ad libitum intake, to 90 lactating rats from d 7 to 14 of lactation. Regression equations developed from lactating rats killed on d 7 of lactation were used to calculate initial body composition and energy of rats killed on d 14 of lactation. Changes in body weight and body water were significantly (P less than 0.05) affected by dietary fat and protein, but change in dry lean body mass was affected only by level of dietary fat, whereas body nitrogen and fat and lean body energy were not affected by level of dietary fat or protein. However, restricted intake significantly increased loss of all these. Likewise, restricted intake decreased milk production. Changes in weights of heart and liver were not affected by diet or intake, whereas intestinal weight decreased with intake restriction. Liver enzyme activities were markedly affected by intake restriction, whereas responses to dietary protein and fat were marginal.     

Maternal zinc deficiency raises plasma prolactin levels in lactating rats

There is an inverse relation between zinc (Zn) intake and plasma prolactin in men and nonpregnant women. Whether a relation exists in lactating women is unknown, despite the potential consequences of perturbations in prolactin regulation on lactation performance. We examined the effects of low Zn intake on prolactin concentration, the prolactin regulatory pathway in the pituitary gland, and lactation performance in lactating rats. Female rats were fed diets containing 7 (zinc deficient; ZD), 10 (marginally zinc deficient; MZD) or 25 mg Zn/kg (control) from 70 d preconception to lactation d 11. Rats were killed, pituitary glands dissected, and tissues and plasma collected and analyzed for prolactin concentration. Pituitary gland pituitary factor 1 (Pit-1), dopamine 2 receptor (D2R), and prolactin receptor mRNA expression were measured in the pituitary gland. Liver, mammary gland, plasma, and milk Zn were measured. Milk intake of the pups was also recorded. Plasma prolactin concentration was higher in rats fed the ZD (125.9 microg/L) diet compared with control rats (21.7 microg/L). Pituitary gland prolactin concentration was higher in rats fed the ZD diet (69.8 mg/g total protein) compared with controls (29.0 mg/g). Plasma Zn concentration was lower in rats fed the MZD and ZD diets, and mammary gland and milk Zn concentrations were lower in rats fed the ZD diet compared with control rats. Rats fed the ZD diet had lower D2R, prolactin receptor, and Pit-1 mRNA levels, whereas rats fed the MZD diet had lower prolactin receptor and Pit-1 mRNA levels compared with control rats. Milk intake was lower in pups of rats fed the MZD and ZD diets. Our results suggest that marginal Zn nutriture may compromise milk production despite increased prolactin levels. In addition, increased circulating prolactin concentration is not due to altered nursing behavior, but may be due to alterations in the prolactin regulatory pathway in the pituitary gland.     

Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat

Rats were fed a diet either deficient (0.05%) in essential fatty acids (EFA), or providing 4% (control) and 10% (surplus) of the total energy intake in the form of linoleic acid. All diets were isoenergetic and provided 13.9% of the energy as fat. The rats were kept at 29 or 5 degrees C. Growth and food intake of rats fed linoleic acid surplus at either temperature for 10 wk were not different from that of controls; basal metabolism, norepinephrine-induced nonshivering thermogenesis (NST) and thermogenic variables in the brown adipose tissue (amount of mitochondria and mitochondrial uncoupling protein) also were not different. The effects of EFA deficiency were drastically enhanced in the cold: After 10 wk of consuming a diet low in EFA at 5 degrees C, the body weight of rats was 75% of that of controls (87% at 29 degrees C); the food intake was 135% of controls at 5 degrees C (120% at 29 degrees C). The resting respiration in deficient rats was 125% of controls at 5 degrees C (110% at 29 degrees C); body temperatures as low as 35.1 degrees C were measured in deficient rats after 3 wk at 5 degrees C; the cold tolerance of the rats was significantly diminished (30% died within 3 wk at 5 degrees C), thus emphasizing the essential role of dietary EFA during cold stress. Norepinephrine-induced NST and the thermogenic parameters in brown fat were not influenced by EFA deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary n-3 fatty acids affect mRNA level of brown adipose tissue uncoupling protein 1, and white adipose tissue leptin and glucose transporter 4 in the rat

We examined the effect of dietary fats rich in n-3 polyunsaturated fatty acids (PUFA) on mRNA levels in white and brown adipose tissues in rats. Four groups of rats were fed on a low-fat diet (20 g safflower oil/kg) or a high-fat diet (200 g/kg) containing safflower oil, which is rich in n-6 PUFA (linoleic acid), or perilla (alpha-linolenic acid) or fish oil (eicosapentaenoic and docosahexaenoic acids), both of which are rich in n-3 PUFA, for 21 d. Energy intake was higher in rats fed on a high-safflower-oil diet than in those fed on low-fat or high-fish-oil diet, but no other significant differences were detected among the groups. Perirenal white adipose tissue weight was higher and epididymal white adipose tissue weight tended to be higher in rats fed on a high-safflower-oil diet than in those fed on a low-fat diet. However, high-fat diets rich in n-3 PUFA, compared to a low-fat diet, did not increase the white adipose tissue mass. High-fat diets relative to a low-fat diet increased brown adipose tissue uncoupling protein 1 mRNA level. The increases were greater with fats rich in n-3 PUFA than with n-6 PUFA. A high-safflower-oil diet, compared to a low-fat diet, doubled the leptin mRNA level in white adipose tissue. However, high-fat diets rich in n-3 PUFA failed to increase it. Compared to a low-fat diet, high-fat diets down-regulated the glucose transporter 4 mRNA level in white adipose tissue. However, the decreases were attenuated with high-fat diets rich in n-3 PUFA. It is suggested that the alterations in gene expression in adipose tissue contribute to the physiological activities of n-3 PUFA in preventing body fat accumulation and in regulating glucose metabolism in rats.     

Effects of dietary trans-fatty acids on reproductive performance of Wistar rats

1. Wistar rats were fed for three successive generations on a semi-purified diet, in which the fat was provided by butter, sunflower oil, rapeseed oil or hydrogenated vegetable fat, differing in the content of cis,cis-18:2 and trans-18:1 fatty acids. Effects of these fats on the composition of adipose tissue and reproductive performance were studied. Fatty acids were analysed using high-performance liquid chromatography. 2. The fatty acid pattern of adipose tissue was closely related to dietary fat composition and, established in the first generation, did not change significantly in successive generations of rats. 3. Hydrogenated fat adversely affected litter size, sperm morphology and regularity of oestrous cycle, and prolonged the period of gestation in experimental animals. Differences observed between the generations were not significant. 4. Hydrogenated fat decreased the level of serum testosterone in males, but the differences observed in levels of serum progesterone in females were not apparently related to the dietary trans-fatty acids.     

High-fat diets affect energy and bone metabolism in growing rats

Background

High-fat diets are usually associated with greater weight (W) gain and body fat (BF). However, it is still unclear whether the type and amount of fat consumed influence BF. Additionally, dietary fat intake may also have consequences on skeletal health.

Objective

To evaluate in healthy growing rats the effects of high-fat diets and type of dietary fat intake (saturated or vegetable oils) on energy and bone metabolism.

Methods

At weaning, male Wistar rats (n?=?50) were fed either a control diet (C; fat?=?7% w/w) or a high-fat diet (20% w/w) containing either: soybean oil, corn oil (CO), linseed oil (LO), or beef tallow (BT) for 8?weeks. Zoometric parameters, BF, food intake and digestibility, and total and bone alkaline phosphatase (b-AP) were assessed. Total skeleton bone mineral density (BMD) and content (BMC), BMC/W, spine BMD, and bone volume (static-histomorphometry) were measured.

Results

Animals fed BT diet achieved lower W versus C. Rats fed high-fat vegetable oil diets showed similar effects on the zoometric parameters but differed in BF. BT showed the lowest lipid digestibility and BMC. In contrast, high vegetable oil diets produced no significant differences in BMC, BMC/W, BMD, spine BMD, and bone volume. Marked differences were observed for LO and BT groups in b-AP and CO and BT groups in bone volume.

Conclusion

BT diet rich in saturated fatty acids had decreased digestibility and adversely affected energy and bone metabolisms, in growing healthy male rats. There were no changes in zoometric and bone parameters among rats fed high vegetable oil diets.     

Maternal brown fat metabolism returns to control level by four weeks postweaning in rats

We studied body composition, white and brown adipose tissue cellularity, lipoprotein lipase activity and metabolic enzyme activity in three groups of rats: nonpregnant controls, lactating dams and nonlactating dams (i.e., dams not permitted to suckle their young). Nine to 11 rats in each group were killed on d 12 postpartum (study d 34) and on d 40 postpartum (study d 62). During lactation, brown fat citrate synthase, beta-hydroxyacylCoA dehydrogenase (HOAD) and lipoprotein lipase activities were significantly lower in the lactating than in the nonlactating dams or virgin controls. Although the nonlactating dams had their pups removed within 24 h after delivery, by d 12 postpartum citrate synthase and HOAD activities were significantly lower than those of nonpregnant controls. By the end of the study there were no differences among the three groups except in the case of HOAD. HOAD activity in the lactation group was significantly lower than in the nonlactation group. White fat cell number in the parametrial depot was significantly increased in the nonlactation groups by d 12 postpartum. In the lactation group, increased white fat cell number in this depot was detectable at d 40 postpartum, when carcass fat stores and fat cells had been repleted. These results demonstrate that both lactating and nonlactating dams undergo cellular hyperplasia, at least in the parametrial depot. This may predispose them to obesity. Also, decreased brown fat metabolism in the nonlactating dams may be contributing to their significantly greater carcass fat content at d 12 postpartum.     

A soyabean diet does not modify the activity of brown adipose tissue but alters the rate of lipolysis in the retroperitoneal white adipose tissue of male rats recovering from early-life malnutrition

Nutritional recovery with a soyabean diet decreases body and fat weights when compared with a casein diet. We investigated whether the reduced adiposity observed in rats recovering from early-life malnutrition with a soyabean diet results from alterations in lipid metabolism in white adipose tissue (WAT) and/or brown adipose tissue (BAT). Male rats from mothers fed either 17 or 6?% protein during pregnancy and lactation were maintained on 17?% casein (CC and LC groups), 17?% soyabean (CS and LS groups) or 6?% casein (LL group) diets over 60?d. The rats maintained on a soyabean diet had similar relative food intakes, but lower body and retroperitoneal WAT weights and a reduced lipid content in the retroperitoneal WAT. The insulin levels were lower in the recovered rats and were elevated in those fed a soyabean diet. Serum T3 concentration and uncoupling protein 1 content in the BAT were decreased in the recovered rats. The thermogenic capacity of the BAT was not affected by the soyabean diet. The lipogenesis rate in the retroperitoneal WAT was similar in all of the groups except for the LL group, which had exacerbated lipogenesis. The enhancement of the lipolysis rate by isoproterenol was decreased in white adipocytes from the soyabean-recovered rats and was elevated in adipocytes from the soyabean-control rats. Thus, in animals maintained on a soyabean diet, the proportions of fat deposits are determined by the lipolysis rate, which differs depending on the previous nutritional status.     

Changes in UCP2, PPARγ2, and C/EBPα Gene Expression Induced by a Neuropeptide Y (NPY) Related Receptor Antagonist in Overweight Rats

Neuropeptide Y (NPY), a peptide released by nervous cells, appears to contribute to adiposity regulation by increasing food intake and inhibiting lipolysis. New NPY receptor related antagonists such as S.A.0204 are being developed as potential anti-obesity drugs affecting adipocyte lipid metabolism and thermogenesis. In this sense, those animals fed on a high-energy yielding (cafeteria) diet decreased body fat weight as compared to overweight controls, when they were administered with S.A.0204, and increased body temperature, which statistically correlated with high UCP2 mRNA expression levels in white adipose tissue. In addition, the in vivo NPY-antagonist administration was able to prevent white adipose tissue growth in animals fed the cafeteria (high-fat) diet by impairing PPARγ and C/EBPα mRNA expression in white fat cells. In summary, this novel NPY related-antagonist S.A.0204 may regulate body fat deposition by affecting both energy dissipation and white adipose tissue deposition, representing a potential new pharmacological strategy for obesity management.