Commercial culture of channel catfish (Ictalurus punctatus) occurs in earthen ponds that are characterized by diel swings in dissolved oxygen concentration that can fall to severe levels of hypoxia, which can suppress appetite and lead to suboptimal growth. Given the significance of the hypothalamus in regulating these processes in other fishes, an investigation into the hypothalamus transcriptome was conducted to identify specific genes and expression patterns responding to hypoxia. Channel catfish in normoxic water were compared with catfish subjected to 12 h of hypoxia (20% oxygen saturation; 1.8 mg O2/L; 27°C) followed by 12 h of recovery in normoxia to mimic 24 h in a catfish aquaculture pond. Fish were sampled at 0-, 6-, 12-, 18-, and 24-h timepoints, with the 6- and 12-h samplings occurring during hypoxia. A total of 190 genes were differentially expressed during the experiment, with most occurring during hypoxia and returning to baseline values within 6 h of normoxia. Differentially expressed genes were sorted by function into Gene Ontology biological processes and revealed that most were categorized as \"response to hypoxia,\" \"sprouting angiogenesis,\" and \"cellular response to xenobiotic stimulus.\" The patterns of gene expression reported here suggest that transcriptome responses to hypoxia are broad and quickly reversibly with the onset of normoxia. Although no genes commonly reported to modulate appetite were found to be differentially expressed in this experiment, several candidates were identified for future studies investigating the interplay between hypoxia and appetite in channel catfish, including adm, igfbp1a, igfbp7, and stc2b.NEW & NOTEWORTHY Channel catfish are an economically important species that experience diel episodic periods of hypoxia that can reduce appetite. This is the first study to investigate their transcriptome from the hypothalamus in a simulated 24-h span in a commercial catfish pond, with 12 h of hypoxia and 12 h of normoxia. The research revealed functional groups of genes relating to hypoxia, angiogenesis, and glycolysis as well as individual target genes possibly involved in appetite regulation.

Attentional biases to food-related stimuli have been demonstrated in response to hunger as well as during restrained eating. Such biases are often associated with obesity, but healthy-weight individuals who do not self-report hunger have also demonstrated attentional biases to stimuli signalling food using laboratory-based cognitive tasks. Levels of the anorectic neuropeptide oxytocin are elevated by food intake and, when administered intranasally, oxytocin inhibits food intake in the laboratory. To investigate whether oxytocin can affect appetite via an action on attentional processes, 40 adults (29 women; mean age 24.0 years old) self-administered 24 IU of oxytocin or placebo intranasally. Forty minutes after administration, participants ate a small snack to maintain alertness and ameliorate deprivation-induced hunger before starting a computerized dot-probe attentional bias task that presented 180 trials of paired visual stimuli comprising neutral, food, social and/or romantic images (500 ms presentation time). Reaction times to probe stimuli that appeared after the offset of the visual images indicated a significant attentional bias to food pictures after placebo; this effect was significantly attenuated by oxytocin, p < .001. The effect of oxytocin on attentional bias to the food pictures was not altered by the type of stimulus paired with the food image, and was independent of BMI, age, sex, self-rated eating behaviour, and self-reported parental bonding; however, the effect was modulated by self-reported food cravings and trait stress. The findings support and extend previous work which has suggested that oxytocin can counteract attentional biases to food-related stimuli in a sample with anorexia by demonstrating the same effect for the first time in a cohort who do not have an eating disorder.

High-intensity exercise can have an anorectic impact, leading to negative energy balance. Several studies have reported that the practice of physical activity could also cause a shift in perceptions and preferences, causing a change in food intakes.
This study aimed to question to what extent the timing of exercise in relation to a meal could have an impact on olfaction and gustation, appetite, and food choices.
Twelve males aged 25 (4) years with a body mass index of 22.4 (2.0) kg/m2 attended two experimental visits in a counterbalanced fashion. The participants consumed a standardized breakfast between 7:00 and 7:30 a.m. and were subjected to smell and taste tests upon arrival at the laboratory (8:30 a.m.). In the EX9:40 visit, the participants performed a 30-min exercise session (70% of maximum oxygen uptake) at 9:40 a.m., followed by a 90-min sedentary break. In EX10:30, the participants first took part in the 90-min sedentary break and then performed the 30-min exercise session at 10:30 a.m. Taste and smell tests were performed again at 11:40 a.m., immediately followed by an ad libitum buffet-style meal. Visual analog scales were used to report appetite sensations during the session and satiety quotients around the lunch.
There was no difference in energy intakes between the EX9:40 (596 [302] kcal) and EX10:30 (682 [263] kcal) conditions (p = .459). There was no condition effect for the taste and smell sensations (all ps > .05), appetite sensation, or satiety quotients around the meal (all ps > .05).
Exercise timing in the morning had no effect on taste and smell perceptions, appetite sensations, or energy intakes.

Intranasal oxytocin produces anorectic effects on snack intake in men when tested in the absence of deprivation-induced hunger, but its effects on food intake in women without eating disorders have not been reported. Oxytocin may reduce food intake by reducing stress eating, since it inhibits ACTH release. The present study adopted a double-blind, repeated measures and fully concealed crossover protocol in which 38 women self-administered 24 IU of oxytocin or placebo intranasally, ate lunch, and underwent two consecutive stress tests. Snack intake was assessed 15-20 min after lunch, via a sham taste test. Salivary cortisol was measured throughout the test period every 15 min. Oxytocin significantly reduced sweet fatty snack intake independently of any effect on salivary cortisol, which declined over time at a similar rate after either drug or placebo. Ratings of sweet taste were slightly reduced by oxytocin, but only in self-reported stress eaters. These results differ from previous studies with men that found an effect of oxytocin on postprandial cortisol levels. However, previous research assayed the less active form of plasma cortisol and did not control for protein intake, which can drive elevated cortisol. The finding that oxytocin reduces snack intake in females after acute stress has important implications for appetite regulation and its treatment in obese people and in those with eating disorders.

Preclinical Research & Development Current drugs for obesity treatment have limited efficacy and considerable adverse effects. Combination of drugs with complementary mechanisms of action at lower doses may produce a greater efficacy with a better safety profile. This study was designed to assess the anorectic effect and safety of a diethylpropion + topiramate mixture in rats. The anorectic effect of drugs was measured using a sweetened milk consumption model, and the corresponding interaction was determined by isobolographic analysis, interaction index and confidence intervals. Additionally, blood pressure was measured using a sphygmomanometer in the rat tail. Diethylpropion and topiramate alone or in combination increased the anorectic effect in a dose-dependent fashion in either nondeprived or 12 hr food-deprived rats. All theoretical ED30 values of diethylpropion + topiramate combinations at 1:1, 1:3, and 3:1 dose ratios were significantly higher than experimental ED30 values. In addition, interaction indices and confidence intervals confirmed the potentiation between both drugs. Theoretical ED30 of diethylpropion + topiramate combination did not affect the blood pressure. Data suggests that low doses of the diethylpropion + topiramate combination can potentiate the anorectic effect of individual drugs with a better safety profile, which deserves further investigation in clinical trials.

Obesity is the most common metabolic disease whose prevalence is increasing worldwide. This condition is considered a serious public health problem due to associated comorbidities such as diabetes mellitus and hypertension. Perinatal morbidity related to obesity does not end with birth; this continues affecting the mother/infant binomial and could negatively impact on metabolism during early infant nutrition. Nutrition in early stages of growth may be essential in the development of obesity in adulthood, supporting the concept of \"nutritional programming\". For this reason, breastfeeding may play an important role in this programming. Breast milk is the most recommended feeding for the newborn due to the provided benefits such as protection against obesity and diabetes. Health benefits are based on milk components such as bioactive molecules, specifically hormones involved in the regulation of food intake. Identification of these molecules has increased in recent years but its action has not been fully clarified. Hormones such as leptin, insulin, ghrelin, adiponectin, resistin, obestatin and insulin-like growth factor-1 copeptin, apelin, and nesfatin, among others, have been identified in the milk of normal-weight women and may influence the energy balance because they can activate orexigenic or anorexigenic pathways depending on energy requirements and body stores. It is important to emphasize that, although the number of biomolecules identified in milk involved in regulating food intake has increased considerably, there is a lack of studies aimed at elucidating the effect these hormones may have on metabolism and development of the newborn. Therefore, we present a state-of-the-art review regarding bioactive compounds such as hormones secreted in breast milk and their possible impact on nutritional programming in the infant, analyzing their functions in appetite regulation.

BACKGROUND: Jojoba butter is cyanogenic and has gained attention among herbal supplement consumers due to claims that it may aid in weight loss. Jojoba butter is extracted from the seeds of jojoba shrubs found in the Sonoran Desert. The seeds have long been recognized as inedible, however clinical symptoms following ingestion are not well documented.
METHODS: This report describes a patient who developed restlessness and gastrointestinal complaints following ingestion of homemade jojoba seed butter. The patient\'s presentation following ingestion is discussed, as well as effective workup and treatment. In our case, the patient was monitored and received fluid resuscitation, lorazepam, and diphenhydramine for symptomatic therapy.
CONCLUSIONS: This case describes the gastrointestinal sequela and effective management following ingestion of jojoba butter.

Sibutramine is an anorectic that has been banned since 2010 due to cardiovascular safety issues. However, counterfeit drugs or slimming products that include sibutramine are still available in the market. It has been reported that illegal sibutramine-contained pharmaceutical products induce cardiovascular crisis. However, the mechanism underlying sibutramine-induced cardiovascular adverse effect has not been fully evaluated yet. In this study, we performed cardiovascular safety pharmacology studies of sibutramine systemically using by hERG channel inhibition, action potential duration, and telemetry assays. Sibutramine inhibited hERG channel current of HEK293 cells with an IC50 of 3.92 μM in patch clamp assay and increased the heart rate and blood pressure (76 Δbpm in heart rate and 51 ΔmmHg in blood pressure) in beagle dogs at a dose of 30 mg/kg (per oral), while it shortened action potential duration (at 10 μM and 30 μM, resulted in 15% and 29% decreases in APD50, and 9% and 17% decreases in APD90, respectively) in the Purkinje fibers of rabbits and had no effects on the QTc interval in beagle dogs. These results suggest that sibutramine has a considerable adverse effect on the cardiovascular system and may contribute to accurate drug safety regulation.

Polypeptides produced in the gastrointestinal tract, stomach, adipocytes, pancreas and brain that influence food intake are referred to as \'feeding-related\' peptides. Most peptides that influence feeding exert an inhibitory effect (anorexigenic peptides). In contrast, only a few exert a stimulating effect (orexigenic peptides), such as ghrelin. Homeostatic feeding refers to when food consumed matches energy deficits. However, in western society where access to palatable energy-dense food is nearly unlimited, food is mostly consumed for non-homeostatic reasons. Emerging evidence implicates the mesocorticolimbic circuitry, including dopamine neurons of the ventral tegmental area (VTA), as a key substrate for non-homeostatic feeding. VTA dopamine neurons encode cues that predict rewards and phasic release of dopamine in the ventral striatum motivates animals to forage for food. To elucidate how feeding-related peptides regulate reward pathways is of importance to reveal the mechanisms underlying non-homeostatic or hedonic feeding. Here, we review the current knowledge of how anorexigenic peptides and orexigenic peptides act within the VTA.

Obesity is a major worldwide public health issue. The physiological systems that regulate body weight are thus of great interest as targets for anti-obesity agents. Peptidergic systems are critical to the regulation of energy homeostasis by key regions in the hypothalamus and brainstem. A number of neuropeptide systems have therefore been investigated as potential treatments for obesity. Blocking orexigenic peptide signals such as neuropeptide Y, melanin-concentrating hormone, orexins, relaxin-3 and galanin-like peptide or stimulating anorectic signalling pathways used by peptides such as the melanocortins, ciliary neurotrophic factor and brain-derived neurotrophic factor, are approaches that have shown some promise, but which have also highlighted possible concerns. Manipulation of central peptidergic systems poses a number of therapeutic problems, including brain access and side effects. Given that the homeostatic defence of body weight may limit the effectiveness of any single-target therapy developed, a combination therapy approach may offer the best hope for the effective prevention and treatment of obesity.
BACKGROUND: This article is part of a themed section on Neuropeptides. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2013.170.issue-7.