Effect of a postnatal high-fat diet exposure on puberty onset,estrous cycle regularity,and kisspeptin expression in female rats

Kisspeptin, encoded by Kiss1, plays a key role in pubertal maturation and reproduction as a positive upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis. To examine the role of high-fat diet (HFD) on puberty onset, estrous cycle regularity, and kisspeptin expression, female rats were exposed to HFD in distinct postnatal periods. Three groups of rats were exposed to HFD containing 60% energy from fat during the pre-weaning period (postnatal day (PND) 1–16, HFD PND 1–16), post-weaning period (HFD PND 21–34), or during both periods (HFD PND 1–34). Puberty onset, evaluated by vaginal opening, was monitored on days 30–34. Leptin, estradiol (E₂), Kiss1 mRNA levels, and number of kisspeptin-immunoreactive cells in the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) were measured at day 34. Body weight increased only in rats exposed to HFD during post-weaning period, whereas the timing of vaginal opening was unaffected in all three groups. Leptin, Kiss1 mRNA levels, and number of kisspeptin-immunoreactive cells at day 34 were not affected by HFD. Additionally, the estrous cycle regularity was monitored in rats exposed to HFD for 40 days from weaning. Leptin, E₂, and Kiss1 mRNA levels in the AVPV and ARC were measured after the HFD exposure. Thirty-three percent of rats exposed to HFD exhibited irregular estrous cycles and a two-fold increase in leptin. By contrast, E₂ level and Kiss1 mRNA levels were not affected by the treatment. These data show that postnatal HFD exposure induced irregular estrous cycles, but had no effect on puberty onset or kisspeptin.     

Relation of changes in amount and type of dietary fat to fecapentaenes in premenopausal women

Correlation studies suggest that fecal mutagenicity is increased in groups eating high-fat diets, the same groups who are often found to have high colorectal cancer incidence and mortality. The fecapentaenes are the best characterized class of fecal mutagens, but the relationship of dietary fat intake to the excretion of these potent genotoxins is unknown. We studied the effect of changes in amount and type of dietary fat on fecapentaene levels in 31 premenopausal women 20-40 years of age who participated in a controlled feeding study. After a pre-diet free-living period lasting 1 menstrual cycle, women were placed on a high-fat (40% energy from fat) diet for 4 menstrual cycles and then switched to a low-fat (20% energy from fat) diet for an additional 4 menstrual cycles. One-half the subjects were maintained throughout the study at a ratio of polyunsaturated-to-saturated fatty acids (P/S ratio) of 1.0, the other half at 0.3; body weight was constant. All meals during the controlled diet periods were prepared at the Human Study Facility of the Beltsville Human Nutrition Research Center. Fecapentaene and fecapentaene precursor levels were measured in acetone extracts from 3-day pooled stool samples collected during the study. No differences in fecapentaene or precursor levels were observed between the high- and low-fat diets at either P/S ratio. Fecapentaene and precursor levels were higher while on controlled diets than during the pre-diet free-living period, and levels declined again in the post-diet free-living period. We conclude that dietary fat has no significant effect on fecapentaene or precursor levels in acetone extracts of stool in premenopausal women. The effect of other dietary or non-dietary factors on fecapentaenes remains unknown.     

Detrimental effects of short-term ethanol exposure on reproductive function in the female rat

To more completely assess the means by which alcohol impairs the female reproductive cycle in rats, we have measured hypothalamic luteinizing hormone-releasing hormone (LHRH), pituitary LHRH receptor content, and the serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (Prl), and progesterone (P). After two successive cycles, the animals began receiving either an alcohol or a isocaloric control liquid diet regimen beginning on the first day of diestrus, with continued monitoring of the estrous cycle throughout the experiment. An additional set of controls consisted of animals maintained on lab chow and water provided ad libitum. Our results indicate that those animals receiving the control diets showed uninterrupted estrous patterns, whereas those animals receiving the alcohol diet remained in diestrus. Additionally, the alcohol-treated animals showed an increase (p less than 0.05) in LHRH content, with a concomitant decrease (p less than 0.01) in serum LH, and an increase (p less than 0.01) in serum Prl. No significant differences were detected in serum FSH levels or pituitary LHRH receptor content. No differences were detected in serum P levels. These results indicate that short-term alcohol administration disrupts the female reproductive cycle, causing persistent diestrus, and support our hypothesis that the alcohol-induced depression in serum LH levels is due to a diminished release rate of hypothalamic LHRH.     

Patterns of gonadotrophin secretion associated with ovulation

A detailed analysis was made of circulating luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin throughout the estrous cycle in rats. Vaginal cytology was recorded daily for 18 or 23 days in 2 groups of adult female rats, 300 and 400 per group. The presence of distended uteri or tubal ova was noted at the time of exsanguination under ether anesthesia. Serum concentrations of LH, FSH, and prolactin were determined by radioimmunoassay. In 404 rats with regular 5-day cycles, all 3 hormones reached maximum concentrations on the afternoon of functional proestrus. During the next 3 days FSH decreased progressively, and LH levels indicated a diurnal fluctuation with minimum concentrations during darkness. Serum prolactin may have b een elevated due to anesthesia and exsanguination and showed a rapid increase which occurred simultaneously with elevated LH and FSH on the afternoon of proestrus. Radioimmunoassay of all 3 hormones indicated that the increases in serum LH and prolactin did not necessarily occur simultaneously. Hypophysectomy and sequential heart puncture of proestrus rats during maximum hormone release showed disappearance rates (half-lives) for LH, FSH, and prolactin of 20, 110, and 13 minutes, respectively.     

Effect of high-fat diet during gestation, lactation, or postweaning on physiological and behavioral indexes in borderline hypertensive rats

Maternal obesity is becoming more prevalent. We used borderline hypertensive rats (BHR) to investigate whether a high-fat diet at different stages of development has adverse programming consequences on metabolic parameters and blood pressure. Wistar dams were fed a high- or low-fat diet for 6 wk before mating with spontaneously hypertensive males and during the ensuing pregnancy. At birth, litters were fostered to a dam from the same diet group as during gestation or to the alternate diet condition. Female offspring were weaned on either control or "junk food" diets until about 6 mo of age. Rats fed the high-fat junk food diet were hyperphagic relative to their chow-fed controls. The junk food-fed rats were significantly heavier and had greater fat pad mass than those rats maintained on chow alone. Importantly, those rats suckled by high-fat dams had heavier fat pads than those suckled by control diet dams. Fasting serum leptin and insulin levels differed as a function of the gestational, lactational, and postweaning diet histories. Rats gestated in, or suckled by high-fat dams, or maintained on the junk food diet were hyperleptinemic compared with their respective controls. Indirect blood pressure did not differ as a function of postweaning diet, but rats gestated in the high-fat dams had lower mean arterial blood pressures than those gestated in the control diet dams. The postweaning dietary history affected food-motivated behavior; junk food-fed rats earned less food pellets on fixed (FR) and progressive (PR) ratio cost schedules than chow-fed controls. In conclusion, the effects of maternal high-fat diet during gestation or lactation were mostly small and transient. The postweaning effects of junk food diet were evident on the majority of the parameters measured, including body weight, fat pad mass, serum leptin and insulin levels, and operant performance.     

高脂饮食联合光照周期改变对不同性别小鼠体重的影响

摘要 目的：随着夜间光照与肥胖现象日趋普遍化,机体内的昼夜节律与生理代谢均受到不同程度的影响,其中不同性别间的差异有待进一步研究。本文旨在通过比较高脂饲料喂养,以及改变光照周期从而对不同性别小鼠体重产生的影响来模拟高脂肪饮食时人类受到夜间光照的性别差异。方法：随机选取C57BL/6小鼠雌鼠、雄鼠各12只,分别按照性别、喂养饲料随机均分成4组,其中随机选取一组雌鼠和一组雄鼠喂养60%高脂饲料作为实验组,另外的一组雌鼠和一组雄鼠喂养普通饲料作为对照组,连续喂养8周,观察并记录各组小鼠体重变化;第1~6周将实验小鼠置于24h/0h光照周期下生活,第6~8周实验小鼠生活的光照周期改为12h/12h。结果：在高脂饲料喂养以及光照周期失调（24h/0h）的条件下,雌、雄鼠体重均有增长（P<0.05）,但雄鼠体重增加量是雌鼠的三倍。当光照周期恢复正常（12h/12h）后,雌、雄小鼠体重增长量均下降。不同性别的小鼠食用高脂饲料以及生物节律被打乱时体重均增加,但雄鼠体重增加量明显大于雌鼠,提示同在高脂饲料饮食的条件下,雌鼠受生物节律影响比雄鼠更大。结论：高脂饮食实验小鼠模型中雌鼠受生物节律的影响比雄鼠更大。     

Effect of a selective OX1R antagonist on food intake and body weight in two strains of rats that differ in susceptibility to dietary-induced obesity

An orexin-1 receptor antagonist decreases food intake whereas orexin-A selectively induces hyperphagia to a high-fat diet. In the present study, we evaluated the effect of an orexin antagonist in two strains of rats that differ in their sensitivity to becoming obese while eating a high-fat diet. Male Osborne-Mendel (OM) and S5B/Pl (S5B) rats were treated acutely with an orexin-1 receptor antagonist (SB-334867), after adaptation to either a high-fat (56% fat energy) diet or a low-fat (10% fat energy) diet that were equicaloric for protein (24% energy). Ad libitum fed rats were injected intraperitoneally with SB-334867 at doses of 3, 10 or 30 mg/kg, or vehicle at the beginning of the dark cycle, and food intake and body weight were measured. Hypothalamic prepro-orexin and orexin-1 receptor mRNA expression were analyzed in OM and S5B rats fed at a high-fat or low-fat diet for two weeks. SB-334867 significantly decreased food intake in both strains of rats eating the high-fat diet but only in the OM rats eating the low fat diet. The effect was greatest at 12 and 24 h. Body weight was also reduced in OM rats 1d after injection of SB-334867 but not in the S5B rats. Prepro-orexin and orexin-1 receptor expression levels did not differ between strains or diets. These experiments demonstrate that an orexin antagonist (SB-334867) reduces food intake and has a greater effect in a rat strain that is susceptible to dietary-induced obesity, than in a resistant strain.     

Glucoprivic regulation of estrous cycles in the rat

Previous research has shown that glucoprivation induced by chronic 2-deoxy-D-glucose (2DG) treatment extends estrous cycle length and disrupts reproductive behaviors in female hamsters, similar to food deprivation. Such treatment also suppresses food intake, which is reversed in male rats by reducing brain histamine levels prior to 2DG treatment. We, therefore, determined if 2DG extends estrous cycles in the female rat and if this is due to elevated brain histamine levels. We measured estrous cycle length during 2DG-induced glucoprivation, in the presence and absence of alpha-fluoromethylhistidine (FMH), a treatment that reduces brain histamine levels. Adult female rats were treated for 72 h with either saline (n = 8), 2DG (200 mg/kg S.C. every 6 h; n = 9), or FMH (100 mg/kg i.p. daily) + 2DG (200 mg/kg; n = 7). An additional group was treated with FMH (100 mg/kg i.p.; n = 5) alone. To determine if 2DG extends estrous cycles due to glucoprivation or to decreased caloric intake, a group of rats (n = 7) received a reduced diet equal to the mean daily food intake of rats receiving 2DG alone. 2DG induced more long estrous cycles compared to rats receiving saline, FMH + 2DG, or FMH alone. In rats treated with FMH + 2DG, the percentage of 4-5-day cycles was similar to that of saline-treated rats, and a high percentage of 4-5-day cycles was also observed in rats receiving a reduced diet. These data suggest that 2DG does not suppress estrous cycles through a decrease in total calorie intake, but rather by inducing glucoprivation. In addition, during 2DG-induced glucoprivation, elevated brain histamine levels contribute to the mechanism that suppresses reproductive function.     

Feeding a corn oil/sucrose-enriched diet enhances steatohepatitis in sedentary rats

The current study investigated the combined effects of feeding a high-fat/high-sucrose (HF/HS) diet to rodents rendered sedentary via hindlimb unloading (HU). For 3 wk before HU, male Wistar rats were fed chow or a diet in which 32% of calories were derived from corn oil fat and 48% of calories from sucrose. Feeding continued during an additional 3-wk period of HU. Subsequently, blood samples were collected for determination of circulating leukocyte counts, insulin levels, and portal vein endotoxin. Inflammation, necrosis, and steatosis were assessed in formalin-fixed liver sections. No biochemical or histological evidence of injury was observed in control rats fed chow or HF/HS. HU increased circulating neutrophils and resulted in hyperinsulinemia. Mild hepatic fat accumulation and minimal focal necroinflammation were observed in this group. Feeding HF/HS during HU exacerbated hyperinsulinemia, hepatic steatosis, Kupffer cell content, and cytokine expression. Significant portal endotoxemia was noted in HU rats but was not influenced by HF/HS diet. On the other hand, feeding HF/HS significantly enhanced lipid peroxidation end products in liver of HU rats by approximately threefold compared with chow-fed rats. In summary, these findings demonstrate that feeding a high-calorie diet potentiates steatosis and injury in sedentary HU rats. Mechanisms underlying enhanced injury most likely involved lipid peroxidation. Importantly, these findings suggest that dietary manipulation combined with physical inactivity can be used to model steatohepatitis.     

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.     

Effect of bromocriptine and progesterone on the length of the ovarian cycle in 4- and 5-day estrous cyclic rats

To study the effect of prolactin and progesterone on the length of the reproductive cycle in the rat, rats of different estrous cycle length (four and five days, respectively) were injected daily (09.00 h) with either bromocriptine (1 mg/rat) or 70% ethanol vehicle (0.25 ml) from the day of estrus onward, up to the appearance of the next ovulation. Each group of rats was then (16.00, metestrus) also injected with either progesterone (4 mg/rat) or 0.2 ml of olive oil. The effects of these treatments on the length of the estrous cycle was studied by both the recording of vaginal smears daily and by direct visualization of oocyte-cumulus complexes on the ensuing day of estrus (10.00 h-12.00 h). Bromocriptine treatment shortened the length of the cycle by one day in 5-day but not in 4-day cyclic rats, while progesterone treatment lengthened estrous cycles by one day in both groups of rats. Treatment with both bromocriptine and progesterone had no effect on the estrous cycle length of 5-day cyclic rats, but did prolong in one day the cycle of 4-day cyclic rats. These facts suggest that prolactin regulates the length of the ovarian reproductive cycle in the rat through its action on the secretion of progesterone by the corpus luteum.     

Antioxidant efficacy of black pepper (Piper nigrum L.) and piperine in rats with high fat diet induced oxidative stress

The present study was aimed to explore the effect of black pepper (Piper nigrum L.) on tissue lipid peroxidation, enzymic and non-enzymic antioxidants in rats fed a high-fat diet. Thirty male Wistar rats (95-115 g) were divided into 5 groups. They were fed standard pellet diet, high-fat diet (20% coconut oil, 2% cholesterol and 0.125% bile salts), high-fat diet plus black pepper (0.25 g or 0.5 g/kg body weight), high-fat diet plus piperine (0.02 g/kg body weight) for a period of 10 weeks. Significantly elevated levels of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and significantly lowered activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) in the liver, heart, kidney, intestine and aorta were observed in rats fed the high fat diet as compared to the control rats. Simultaneous supplementation with black pepper or piperine lowered TBARS and CD levels and maintained SOD, CAT, GPx, GST, and GSH levels to near those of control rats. The data indicate that supplementation with black pepper or the active principle of black pepper, piperine, can reduce high-fat diet induced oxidative stress to the cells.     

Programmed metabolic syndrome: prenatal undernutrition and postweaning overnutrition

Maternal nutrient restriction results in intrauterine growth restriction (IUGR) newborns that develop obesity despite normal postweaning diet. The epidemic of metabolic syndrome is attributed to programmed "thrifty phenotype" and exposure to Western diets. We hypothesized that programmed IUGR newborns would demonstrate greater susceptibility to obesity and metabolic abnormalities in response to high-fat diet. From day 10 to term gestation and lactation, control pregnant rats received ad libitum (AdLib) food, whereas study rats were 50% food restricted (FR). Cross-fostering techniques resulted in three offspring groups: control (AdLib/AdLib), FR during pregnancy (FR/AdLib), and FR during lactation (AdLib/FR). At 3 weeks, offspring were weaned to laboratory chow or high-fat calorie diet (9% vs. 17% calorie as fat). Body composition, appetite hormones, and glucose and lipid profiles were determined in 9-mo-old male and female offspring. High-fat diet had no effect on body weight of AdLib/AdLib, but significantly increased weights of FR/AdLib and AdLib/FR offspring. High-fat diet significantly increased body fat, reduced lean body mass, and accentuated plasma leptin but not ghrelin levels in both sexes in all groups. In males, high-fat diet caused a significant increase in glucose levels in all three groups with increased insulin levels in AdLib/AdLib and AdLib/FR, but not in FR/AdLib. In females, high-fat diet had no effect on glucose but significantly increased basal insulin among all three groups. High-fat diet caused hypertriglyceridemia in all three groups although only food-restricted females exhibited hypercholesterolemia. Sex and offspring phenotype-associated effects of high-fat diet indicate differing pathophysiologic mechanisms that require specific therapeutic approaches.     

Ghrelin secretion is not reduced by increased fat mass during diet-induced obesity

Ghrelin is a stomach hormone that stimulates growth hormone (GH) secretion, adiposity, and food intake. Gastric ghrelin production and secretion are regulated by caloric intake; ghrelin secretion increases during fasting, decreases with refeeding, and is reduced by diet-induced obesity. The aim of the present study was to test the hypotheses that 1) an increase in body adiposity will play an inhibitory role in the reduction of gastric ghrelin synthesis and secretion during chronic ingestion of a high-fat (HF) diet and 2) chronic ingestion of an HF diet will suppress the rise in circulating ghrelin levels in response to acute fasting. Adult male Sprague-Dawley rats were fed a standard AIN-76A (approximately 5-12% of calories from fat) or an HF (approximately 45% of calories from fat) diet. The effect of increased adiposity on gastric ghrelin homeostasis was assessed by comparison of stomach ghrelin production and plasma ghrelin levels in obese and nonobese rats fed the HF diet. HF diet-fed, nonobese rats were generated by administration of triiodothyronine to lower body fat accumulation. Our findings indicate that an increased fat mass per se does not exert an inhibitory effect on ghrelin homeostasis during ingestion of the HF diet. Additionally, the magnitude of change in plasma ghrelin in response to fasting was not blunted, indicating that a presumed, endogenous signal for activation of ingestive behavior remains intact, despite excess stored calories in HF-fed rats.     

High-fat diets rich in soy or fish oil distinctly alter hypothalamic insulin signaling in rats

Hypothalamic insulin inhibits food intake, preventing obesity. High-fat feeding with polyunsaturated fats may be obesogenic, but their effect on insulin action has not been elucidated. The present study evaluated insulin hypophagia and hypothalamic signaling after central injection in rats fed either control diet (15% energy from fat) or high-fat diets (50% energy from fat) enriched with either soy or fish oil. Soy rats had increased fat pad weight and serum leptin with normal body weight, serum lipid profile and peripheral insulin sensitivity. Fish rats had decreased body and fat pad weight, low leptin and corticosterone levels, and improved serum lipid profile. A 20-mU dose of intracerebroventricular (ICV) insulin inhibited food intake in control and fish groups, but failed to do so in the soy group. Hypothalamic protein levels of IR, IRS-1, IRS-2, Akt, mTOR, p70S6K and AMPK were similar among groups. ICV insulin stimulated IR tyrosine phosphorylation in control (68%), soy (36%) and fish (34%) groups. Tyrosine phosphorylation of the pp185 band was significantly stimulated in control (78%) and soy (53%) rats, but not in fish rats. IRS-1 phosphorylation was stimulated only in control rats (94%). Akt serine phosphorylation was significantly stimulated only in control (90%) and fish (78%) rats. The results showed that, rather than the energy density, the fat type was a relevant aspect of high-fat feeding, since blockade of hypothalamic insulin signal transmission and insulin hypophagia was promoted only by the high-fat soy diet, while they were preserved in the rats fed with the high-fat fish diet.     

Effects of diet and exposure to hindlimb suspension on estrous cycling in Sprague-Dawley rats

Various factors can disrupt the female reproductive cycle resulting in subfertility. The primary objective of this study was to determine whether physiological changes associated with exposure to hypogravity disrupt reproductive cycles. The hindlimb suspension (HLS) model was used to simulate the major physiological effects of hypogravity in female Sprague-Dawley rats. Also, to determine whether diet may influence reproductive results, rats were fed purified American Institute of Nutrition (AIN)-93G or chow diet. Rats (n = 9-11/group) subjected to HLS had lengthened estrous cycles due to prolonged diestrus, indicating hypoestrogenism. Interestingly, HLS rats fed AIN-93G but not chow diet had significantly reduced time spent in estrus and decreased plasma estradiol. Attenuation of hypoestrogenism in the chow-fed rats suggested that diet provided an exogenous source of estrogen. The mechanism involved in the disruption of estrous cycling remains to be determined. HLS increased urinary corticosterone (CORT) levels during the initial 4 days of HLS, suggesting that physiological responses to acute stress may be a potential mechanism in the disruption of estrous cycles. Higher basal urinary CORT was observed in rats fed chow vs. AIN-93G diet. HLS resulted in increased urinary CORT. However, two-way ANOVA indicated a significant HLS effect (P < 0.001) but no effect of HLS x diet effect on urinary CORT levels, suggesting that estrogenic activity associated with the chow diet did not enhance the stress response. The results of this study indicate that HLS, diet, and the combination of HLS and diet influence estrous cycling. This has important implications for future reproductive success in the hypogravity environment of space.     

The effect of high-fat diet on plasma ghrelin and leptin levels in rats

Ghrelin and leptin regulate appetite and energy homeostasis in humans and rodents. The effects of different nutritional factors on ghrelin and leptin secretion are not well documented in rats. Therefore, the aim of our study was to investigate the effect of a high-fat diet on plasma ghrelin and leptin levels and on adiposity. Twenty male Wistar rats, body weight220–260 g, were used in the study. Rats were randomized either on a standard chow diet (n=10) or on a high-fat diet (a mixture of nuts) forad libitum 11-week period. Body weight was measured once per week. At the end of the nutritional period, rats were sacrificed. Blood was collected for determination of lipids and glucose, as well as plasma ghrelin and leptin levels by ELISA method. The weight of different organs was determined. Rats fed on a high-fat diet showed significant increase in total body weight compared to control group. The long-term intake of high-fat diet caused hyperleptinemia and hypoghrelinemia. There was a significant positive correlation between plasma leptin levels and epididymal fat mass, liver and heart. In contrast, ghrelin levels showed inverse correlation with epididymal fat mass and liver weight. In conclusion, long-term intake of high-fat diet induced changes in plasma ghrelin and leptin in male rats, as well as in epididymal fat mass, liver and heart weights.     

The effects of paradoxical sleep deprivation on estrous cycles of the female rats

The present purpose was to examine how sleep deprivation affects the estrous cycle of the female rat. Paradoxical sleep-deprived (PSD) adult female Wistar rats were compared to home-cage control (CTRL) on their estrous cyclicity. Forty-four PSD and forty-four CTRL female rats were distributed into 4 subgroups of 11 animals each according to the phase of estrous cycle and were subjected to sleep deprivation for 96 h by the multiple platform technique. After PSD period, vaginal estrous cycles were taken for an additional 9 days. Animals that were submitted to PSD in diestrus phase (PSD-diestrus) had their estrous cycles disrupted during the recovery period by showing a constant diestrus during the first week. As for hormone alterations, progesterone concentrations were statistically higher in PSD-diestrus compared to respective phase control and to PSD-proestrus and PSD-estrus rats while CTRL-metestrus had higher levels than CTRL-proestrus and estrus groups. Testosterone was significantly decreased in PSD-estrus in relation to PSD-proestrus and PSD-diestrus groups and was lower in CTRL-diestrus rats than in home-cage rats in proestrus. In addition, PSD-diestrus phase exhibited higher concentrations of corticosterone and lower estrogen than the respective control rats. These data indicate that PSD may modulate the ovarian hormone release through alterations in hormonal-neurochemical mechanisms.     

Effects of Arachis hypogaea nutshell extract on lipid metabolic enzymes and obesity parameters

The aim of the present study was to assess the effects of peanut (Arachis hypogaea L.) shell extracts (PSE) on lipases and to evaluate its potential development for the treatment of obesity. The peanut shells were extracted in 95% ethanol, and the extracts were screened for inhibitory effects on pancreatic lipase (PL) and lipoprotein lipase (LPL) activities as well as on lipolysis of 3T3-L1 adipocytes. We also examined in vivo whether PSE could prevent the body weight gain induced by feeding a high-fat diet to male Wistar rats for 12 weeks. PSE inhibits a number of lipases, including PL, LPL and, possibly, hormone sensitive lipase (HSL). PSE-treated Wistar rats showed increased fecal lipid excretion respect to the control group. Body weight and body weight gain, and liver size, were significantly lower in rats fed the high-fat diet with 1% of PSE (w:w diet) than in those fed the high-fat diet alone. The rats treated with PSE showed reduced triacylglycerol content in the liver, as well as the serum glucose and insulin. The inhibitory activity of PSE on the lipid metabolic enzymes and the increase in fecal fat excretion suggests that PSE might be useful as a treatment to reduce the dietary fat absorption. The observed reduction in intracellular lipolytic activity of cultured 3T3-L1 adipocytes may reduce the levels of circulating free fatty acids. The observed effects are likely induced by more than one bioactive component of PSE. The PSE actions may, at least in part, be attributed to the inhibition of fat absorption in the digestive tract and the reduction of the adipocyte lipolysis.     

Differences in the response pattern of aged female rats to treatment with lergotrile mesylate

Old female rats exhibiting either the constant vaginal estrous (CE) or the prolonged diestrous (PD) state were given lergotrile mesylate (LM). Treatment with 4.5 mg/kg daily significantly reduced prolactin (PRL) levels in both groups. The basal luteinizing hormone (LH) levels were not altered. In the CE group, LM treatment produced a single prolonged cycle, with the reemergence of the CE state. However, in the PD group, the rats exhibited several regular cycles during the treatment period. Several of these rats also showed evidence of having an LH surge during the reinduced cycle. These results suggest that high PRL levels may be a causative factor with respect to acyclicity in the PD rats, but PRL does not seem to be a major contributor to acyclicity in the aged CE rat.