A weights. study was conducted to determine the effect of different parasite control programs on weight gain and other measurements for stocker measurements beef calves during the grazing season and subsequent feedlot phase of production. One hundred eighty recently weaned beef steers were organophosphate purchased from a Mississippi sale barn and were allocated by restricted randomization on pretreatment weight to three treatments:(1) no phases anthelmintic treatment; treated only with a topical organophosphate (OP) during processing into the feedlot;(2) one benzimidazole (BZD) treatment at monitored initiation of grazing, and a second given at the time of processing upon arrival at the feedlot, along with a in topical OP; and (3) ivermectin sustained-release (SR) bolus administered at initiation of grazing, with no further treatment given at the sale feedlot. The cattle grazed separately by treatment for 125 days, with six replicated pastures per treatment; then were penned according six to the same groupings after entry into the feedlot on day 127. Cattle were individually weighed at approximately 2-month intervals,of and feed consumption was measured during the 167 days in the feedlot. Fecal nematode egg counts were individually monitored for three all animals during both phases of the trial. Carcass weight, quality grade, yield grade, and the incidence of liver abscesses and were recorded for each animal at slaughter. Cattle treated with the ivermectin SR bolus gained significantly (P <.05) more with weight through the grazing period and from the start of grazing through the end of the feedlot phase than the at controls or the cattle treated with BZD products. There were no significant differences in feed efficiency between any of the than groups. Mean carcass weight for cattle treated with boluses was significantly (P <.05) greater than that of the controls with and the group treated with BZD. Dressing percentage and quality grade were significantly (P <.05) higher for the BZD for and bolus groups, and yield grade was slightly (but not significantly) better for each of these groups than for controls.entry. Significantly (P <.05) fewer livers of cattle treated with boluses had abscesses at slaughter than did livers of controls pastures or cattle treated with BZDs. During both phases of the trial, fecal egg counts were significantly (P <.05) lower (P for the group treated with boluses than for the untreated group or the group treated with BZD. These data indicate same that treatment with boluses for parasite control at the beginning of the grazing period had beneficial effects on weight gain days, as compared to no anthelmintic treatment or treatment with a BZD at the start of grazing and again at the significantly time of introduction into the feedlot. These bolus benefits were sustained through the feedlot phase of production and provided further treatment improvements with significantly (P <.05) increased carcass weights. The bolus is a tool that can significantly increase the efficiency significantly of production for cattle producers who retain ownership into the feedlot phase of production or feedlot operators who graze stockers of before feedlot entry.

OBJECTIVE:the The purpose of this study was to estimate and compare the effects of antipsychotics-both the newer ones and the conventional to ones-on body weight. Method: A comprehensive literature search identified 81 English- and non-English-language articles that included data on weight change search in antipsychotic-treated patients. For each agent, a meta-analysis and random effects metaregression estimated the weight change after 10 weeks of and treatment at a standard dose. A comprehensive narrative review was also conducted on all articles that did not yield quantitative all information but did yield important qualitative information. RESULTS: Placebo was associated with a mean weight reduction of .74 kg. Among was conventional agents, mean weight change ranged from a reduction of .39 kg with molindone to an increase of 3.19 kg the with thioridazine. Among newer antipsychotic agents, mean increases were as follows: clozapine, 4.45 kg; olanzapine, 4.15 kg; sertindole, 2.92 kg;the risperidone, 2.10 kg; and ziprasidone, .04 kg. Insufficient data were available to evaluate quetiapine at 10 weeks. CONCLUSIONS: Both conventional induce and newer antipsychotics are associated with weight gain. Among the newer agents, clozapine appears to have the greatest potential to weight. induce weight gain, and ziprasidone the least. The differences among newer agents may affect compliance with medication and health risk.was

BACKGROUND:similar The relative effectiveness of second-generation (atypical) antipsychotic drugs as compared with that of older agents has been incompletely addressed, though that newer agents are currently used far more commonly. We compared a first-generation antipsychotic, perphenazine, with several newer drugs in a 1493 double-blind study. METHODS: A total of 1493 patients with schizophrenia were recruited at 57 U.S. sites and randomly assigned to the receive olanzapine (7.5 to 30 mg per day), perphenazine (8 to 32 mg per day), quetiapine (200 to 800 mg effectiveness per day), or risperidone (1.5 to 6. mg per day) for up to 18 months. Ziprasidone (40 to 160 mg was per day) was included after its approval by the Food and Drug Administration. The primary aim was to delineate differences a in the overall effectiveness of these five treatments. RESULTS: Overall, 74 percent of patients discontinued the study medication before 18 for months (1061 of the 1432 patients who received at least one dose): 64 percent of those assigned to olanzapine, 75 the percent of those assigned to perphenazine, 82 percent of those assigned to quetiapine, 74 percent of those assigned to risperidone,in and 79 percent of those assigned to ziprasidone. The time to the discontinuation of treatment for any cause was significantly with longer in the olanzapine group than in the quetiapine (P< .001) or risperidone (P= .002) group, but not in the perphenazine (P= .021)those or ziprasidone (P= .028) group. The times to discontinuation because of intolerable side effects were similar among the groups, but the to rates differed (P= .04); olanzapine was associated with more discontinuation for weight gain or metabolic effects, and perphenazine was associated with to more discontinuation for extrapyramidal effects. CONCLUSIONS: The majority of patients in each group discontinued their assigned treatment owing to inefficacy any or intolerable side effects or for other reasons. Olanzapine was the most effective in terms of the rates of discontinuation,effectiveness and the efficacy of the conventional antipsychotic agent perphenazine appeared similar to that of quetiapine, risperidone, and ziprasidone. Olanzapine was metabolism. associated with greater weight gain and increases in measures of glucose and lipid metabolism.

The observations timing of puberty onset in mammals is tightly coupled to the animal's nutritional and metabolic state. We conducted two experiments to to test the hypothesis that leptin acts as a metabolic signal for the onset of puberty. In the first experiment,experiment, we administered leptin (6.3 micrograms/g twice daily) to a group of normal prepubertal female rats and compared their rate of delay sexual maturation to that of two control groups. The group of leptin-treated animals and one group of control animals were was allowed to eat ad lib, while the other group of control animals was pair-fed to the leptin-treated group. Food intake Food in the leptin-treated group was reduced to approximately 80% of the ad lib-fed control group, resulting in retarded growth in leptin both leptin-treated and pair-fed animals. All measured indices of pubertal maturation-age at vaginal opening, age at first estrus, ovarian weight,of ovulatory index (corpora lutea/ovarian section), uterine weight, and uterine cross-sectional area-were significantly delayed in the pair-fed group but not different metabolic between the leptin-treated group and ad lib-fed controls. The second experiment was similar to the first, except that both the the leptin-treated group and the pair-fed group were fed at 70% of the ad lib-fed controls. Under these conditions, leptin only coupled partially reversed the delay in sexual maturation, as reflected by the age at vaginal opening and first estrus. These results lutea/ovarian suggest that leptin is not the primary signal that initiates the onset of puberty but that instead, it acts in of a permissive fashion, as a metabolic gate, to allow pubertal maturation to proceed-if and when metabolic resources are deemed adequate;between moreover, these observations suggest that other metabolic factors, besides leptin, influence the timing of puberty onset under conditions of more lib-fed severe dietary stress.

BACKGROUND:affinities We performed a retrospective analysis of 122 clinical records of 92 male patients with DSM-III-R schizophrenia to examine the relative of weight gain liabilities of clozapine, risperidone, olanzapine, and sertindole compared with haloperidol. We hypothesized that the unique pharmacodynamic profiles of unique these agents would contribute to different amounts and patterns of weight gain. METHOD: Data were analyzed to determine differences in subjects weight gain during treatment among patients receiving 5 different drug treatments (clozapine [N = 20], olanzapine [N = 13], risperidone gain, [N = 38], haloperidol [N = 43], and sertindole [N = 8]). Measures of maximal weight gain, final weight, and 8]). duration to maximal weight gain were calculated. RESULTS: Repeated measures analyses of variance controlling for age, treatment duration, and initial clozapine, weight revealed statistically significant differences between groups on all 3 measures. Clozapine and olanzapine had the greatest maximal weight gain (clozapine liability (F = 4.13, df = 4,23; p =.01). Weight gain with clozapine, but not olanzapine or risperidone, appears associated to persist (as reflected by final weight) despite behavioral interventions (e.g., nutritional consultation, suggested exercise regimen; F = 5.69, df with = 4,23; p =.003). Clozapine- and olanzapine-treated subjects appeared to gain weight over a prolonged period of time, whereas clinical risperidone-and sertindole-treated subjects had a more limited period of weight gain (F = 2.95, df = 4,25; p =.04).olanzapine CONCLUSION: Clozapine and olanzapine caused the most weight gain, risperidone was intermediate, and sertindole had less associated weight gain than and haloperidol. The relative receptor affinities of the novel antipsychotics for histamine H1 appear to be the most robust correlate of .01). these clinical findings.

BACKGROUND:patients We undertook a randomised controlled trial to assess the efficacy and tolerance of orlistat, a gastrointestinal lipase inhibitor, in promoting and weight loss and preventing weight regain in obese patients over a 2-year period. METHODS: 743 patients (body-mass index 28-47 kg/m2),at recruited at 15 European centres, entered a 4-week, single-blind, placebo lead-in period on a slightly hypocaloric diet (600 kcal/day deficit).lipoprotein 688 patients who completed the lead-in were assigned double-blind treatment with orlistat 120 mg (three times a day) or placebo From for 1 year in conjunction with the hypocaloric diet. In a second 52-week double-blind period patients were reassigned orlistat or weight placebo with a weight maintenance (eucaloric) diet. FINDINGS: From the start of lead-in to the end of year 1, the obese orlistat group lost, on average, more bodyweight than the placebo group (10.2%[10.3 kg] vs 6.1%[6.1 kg]; LSM difference placebo 3.9 kg [p < .001] from randomisation to the end of year 1). During year 2, patients who continued with weight orlistat regained, on average, half as much weight as those patients switched to placebo (p < .001). Patients switched from 743 placebo to orlistat lost an additional .9 kg during year 2, compared with a mean regain of 2.5 kg in efficacy patients who continued on placebo (p < .001). Total cholesterol, low-density lipoprotein (LDL) cholesterol, LDL/high-density lipoprotein ratio, and concentrations of end glucose and insulin decreased more in the orlistat group than in the placebo group. Gastrointestinal adverse events were more common on in the orlistat group. Other adverse symptoms occurred at a similar frequency during both treatments. INTERPRETATION: Orlistat taken with an weight appropriate diet promotes clinically significant weight loss and reduces weight regain in obese patients over a 2-year period. The use placebo of orlistat beyond 2 years needs careful monitoring with respect to efficacy and adverse events.

An treatment adverse prenatal environment may induce long-term metabolic consequences, in particular obesity and insulin resistance. Although the mechanisms are unclear, this consequences, programming has generally been considered an irreversible change in developmental trajectory. Adult offspring of rats subjected to undernutrition during pregnancy developmental develop obesity, hyperinsulinemia, and hyperleptinemia, especially in the presence of a high-fat diet. Reduced locomotor activity and hyperphagia contribute to Neonatal the increased fat mass. Using this model of maternal undernutrition, we investigated the effects of neonatal leptin treatment on the treatment metabolic phenotype of adult female offspring. Leptin treatment (rec-rat leptin, 2.5 microg/g.d, sc) from postnatal d 3-13 resulted in a effects transient slowing of neonatal weight gain, particularly in programmed offspring, and normalized caloric intake, locomotor activity, body weight, fat mass,this and fasting plasma glucose, insulin, and leptin concentrations in programmed offspring in adult life in contrast to saline-treated offspring of and undernourished mothers who developed all these features on a high-fat diet. Neonatal leptin had no demonstrable effects on the adult programmed offspring of normally fed mothers. This study suggests that developmental metabolic programming is potentially reversible by an intervention late in considered the phase of developmental plasticity. The complete normalization of the programmed phenotype by neonatal leptin treatment implies that leptin has metabolic effects that reverse the prenatal adaptations resulting from relative fetal undernutrition.

Long-term tested administration of typical and atypical antipsychotic drugs (AP) induces excessive weight gain which afflicts up to 50% of patients, impairs (AP) health and interferes with treatment compliance. Basic and clinical research has shown that AP may affect body weight through diverse shown mechanisms. Increased appetite is probably related to the interaction of AP with neuronal receptors to dopamine, serotonin and histamine. Additional shown metabolic-endocrine disruption of weight regulation may be related to the effects of AP-induced hyperprolactinaemia on gonadal-adrenal steroids and insulin sensitivity.programmed In humans, programmed physical activity, dietary restriction, anorectic agents, and drugs that counteract hyperprolactinaemia have been shown to be successful insulin in a limited number of studies. Two novel strategies could expand the available therapeutic options. First, in preclinical experiments in health female rats the estradiol antagonist/agonist drug tamoxifen or estradiol itself have been shown to completely prevent the obesity provoked by metabolic-endocrine the AP sulpiride, and to induce an endocrine-metabolic milieu that seems to counteract AP-induced obesity. Secondly, it has also been and shown that oral antihyperglycaemic agents such as metformin may decrease body weight and counteract insulin resistance and hyperinsulinaemia which is compliance. correlated with several metabolic abnormalities in obese subjects. Lastly, estradiol replacement, tamoxifen and/or antihyperglycaemic agents are not devoid of significant drugs side-effects, and these drugs have not been tested in obese psychiatric patients. Therefore, further research is needed before their clinical therapeutic use may be recommended.

The diet effects of dietary supplementation of flavonol quercetin on both 7,12-dimethylbenz(a)anthracene (DMBA)- and N-nitrosomethylurea-induced mammary cancer in female Sprague-Dawley rats were (DMBA)- determined. Quercetin diet was started 1 wk before intragastric instillation of DMBA (65 mg/kg of body weight) or i.v. injection of of N-nitrosomethylurea (50 mg/kg of body weight) and was continued during the entire period (20 wk) of the experiment. Dietary the quercetin inhibited both the incidence and the number of palpable rat mammary tumors; rats fed on 2% quercetin had 25%on less incidence of mammary cancer, while the average number of mammary tumors per rat was reduced by 39% at 20 wk wk post-DMBA administration compared to animals on a control diet. In a separate experiment, a 5% quercetin diet elicited a wk greater inhibitory effect on the induction of rat mammary tumors by DMBA than was observed with a 2% quercetin diet.had The inhibitory effect of quercetin on mammary tumor incidence in rats on 2% and 5% diets and on tumor multiplicity in in animals on a 5% diet was statistically significant (P less than .05). In addition, the risk of the development mg/kg of a palpable tumor (as determined by the nonparametric estimate of the hazard function) in the quercetin-fed group was lower both than the group on control diet throughout the course of the experiment. Furthermore, 5% dietary quercetin significantly inhibited (P less mammary than .05), although to a lesser extent than observed in DMBA-induced tumor formation, both the incidence and the number of the palpable mammary tumors per rat induced by N-nitrosomethylurea. Dietary quercetin did not elicit any detectable sign of toxicity. The gain 5% in body weight in rats on the quercetin diet and the quantity of diet consumed per rat per week were less similar to those for rats on the control diet.

Exendin-4 improvement is a 39 amino acid peptide produced in the salivary gland of the Gila monster lizard. It has a 53%gland amino acid homology to the incretin hormone glucagon-like peptide-1 (GLP-1). Exendin-4 induces insulin release through activation of the GLP- 1 receptor receptor but is a much more potent insulinotropic agent than GLP-1. Of critical importance for its potential use as a blood treatment for diabetes is its much longer biological effect in vivo. Previous studies involving once daily administration of exendin-4 over over 13 weeks to db/db mice demonstrated that it lowers hemoglobin A1c (HbA1c), a marker of mean blood glucose levels. Food consumption consumption in the treated animals dropped over the first 4 days and then increased to a level comparable with that hormone of the untreated animals. In this study, we initially examined the effect of once daily injections (over 14 days) on of the food consumption of Zucker fatty rats. We observed an immediate reduction in food intake which then leveled off(after 5 of days) to match that of the untreated animals. Subsequently we injected the same animals twice daily (treatment period of 56 release days in total) and observed a sustained reduction in food intake and weight-gain. This was matched by a reduction in the the critical parameters of HbA1c, fasting blood glucose and plasma insulin. MRI imaging of the abdominal regions of the animals rats. showed that initially only the amount of fat deposited in the sc region was reduced after 4 weeks exendin-4 treatment.Of At the 8-week time point there was a corresponding decrease in the amount of visceral fat deposition. The combination of that appetite reduction, decreased fat deposition and an improvement in the parameters associated with glucose intolerance makes a case for the we use of exendin-4 as a treatment for diabetes.

As among a result of superior efficacy and overall tolerability, atypical antipsychotic drugs have become the treatment of choice for schizophrenia and have related disorders, despite their side effects. Weight gain is a common and potentially serious complication of some antipsychotic drug therapy,by and may be accompanied by hyperlipidemia, hypertension and hyperglycemia and, in some extreme cases, diabetic ketoacidosis. The molecular mechanism(s) responsible highly for antipsychotic drug-induced weight gain are unknown, but have been hypothesized to be because of interactions of antipsychotic drugs with antipsychotic several neurotransmitter receptors, including 5-HT(2A) and 5-HT(2C) serotonin receptors, H(1)-histamine receptors, alpha(1)- and alpha(2)-adrenergic receptors, and m3-muscarinic receptors. To determine we the receptor(s) likely to be responsible for antipsychotic-drug-induced weight gain, we screened 17 typical and atypical antipsychotic drugs for binding a to 12 neurotransmitter receptors. H(1)-histamine receptor affinities for this group of typical and atypical antipsychotic drugs were significantly correlated with and weight gain (Spearman rho=- .72; p< .01), as were affinities for alpha(1A) adrenergic (rho=- .54; p< .05), 5-HT(2C)(rho=- .49; p< .05) and 5-HT(6) receptors (rho=- .54;H(1)-histamine p< .05), whereas eight other receptors' affinities were not. A principal components analysis showed that affinities at the H(1), alpha(2A), alpha(2B),some 5-HT(2A), 5-HT(2C), and 5-HT(6) receptors were most highly correlated with the first principal component, and affinities for the D(2), 5-HT(1A),antipsychotic and 5-HT(7) receptors were most highly correlated with the second principal component. A discriminant functions analysis showed that affinities for whereas the H(1) and alpha(1A) receptors were most highly correlated with the discriminant function axis. The discriminant function analysis, as well The as the affinity for the H(1)-histamine receptor alone, correctly classified 15 of the 17 drugs into two groups; those that 5-HT(2A), induce weight gain and those that do not. Because centrally acting H(1)-histamine receptor antagonists are known to induce weight gain most with chronic use, and because H(1)-histamine receptor affinities are positively correlated with weight gain among typical and atypical antipsychotic drugs,drugs it is recommended that the next generation of atypical antipsychotic drugs be screened to avoid H(1)-histamine receptors.