Compensatory Increase In Food Intake Research Articles

Exercise and the Timing of Snack Choice: Healthy Snack Choice is Reduced in the Post-Exercise State.

Acute exercise can induce either a compensatory increase in food intake or a reduction in food intake, which results from appetite suppression in the post-exercise state. The timing of food choice—choosing for immediate or later consumption—has been found to influence the healthfulness of foods consumed. To examine both of these effects, we tested in our study whether the timing of food choice interacts with exposure to exercise to impact food choices such that choices would differ when made prior to or following an exercise bout. Visitors to a university recreational center were equipped with an accelerometer prior to their habitual workout regime, masking the true study purpose. As a reward, participants were presented with a snack for consumption after workout completion. Participants made their snack choice from either an apple or chocolate brownie after being pseudo-randomly assigned to choose prior to (“before”) or following workout completion (“after”). Complete data were available for 256 participants (54.7% male, 22.1 ± 3.1 years, 24.7 ± 3.7 kg/m2) who exercised 65.3 ± 22.5 min/session. When compared with “before,” the choice of an apple decreased (73.7% vs. 54.6%) and the choices of brownie (13.9% vs. 20.2%) or no snack (12.4% vs. 25.2%) increased in the “after” condition (χ2 = 26.578, p < 0.001). Our results provide support for both compensatory eating and exercise-induced anorexia. More importantly, our findings suggest that the choice of food for post-exercise consumption can be altered through a simple behavioral intervention.

Changes in Energy Balance during Dapagliflozin Therapy in Type 2 Diabetes—The Energize Study

Weight loss during SGLT2i therapy is less than predicted from urinary glucose loss. Modelling suggests a 10-15% compensatory increase in energy intake. We compared effects of 12 weeks’ dapagliflozin 10mg od vs. placebo on food intake in a double-blind, placebo-controlled study with short (1 week) and long-term (12 week) crossover periods. Food intake was measured during test meals at baseline, pre and post each crossover using the Sussex Ingestion Pattern Monitor, continuously recording intake during the meal; primary outcome was the difference after 12 weeks’ treatment. 52 patients with T2DM treated with diet or oral agents were recruited (45 completed;43% female). Median age 60y, weight 98.4 kg, BMI 34, HbA1c 59.5 mmol/mol. Analysis used a linear mixed model with the random effect as study subject and fixed effects of sex, visit, study arm and arm:visit interaction. Dapagliflozin use was associated with a reduction in HbA1c -9.73mmol/mol (95% CI 3.91, 16.27; p=0.004), and body weight (-2.84 vs. -0.87 kg) vs. placebo. There was no difference in test meal food intake between dapagliflozin and placebo at 12 weeks median difference, 2.63g (95% CI,-31.65,36.9); p=0.659 or at other time points. Dapagliflozin was not associated with a compensatory increase in food intake. Disclosure S. Rajeev: None. C.A. Roberts: None. D.J. Cuthbertson: None. V.S. Sprung: None. E. Brown: Research Support; Self; AstraZeneca. J.C. Halford: Advisory Panel; Self; Novo Nordisk A/S. Speaker's Bureau; Self; Novo Nordisk A/S. J.A. Harrold: None. G.J. Kemp: None. A. Stancak: None. J.P. Wilding: Other Relationship; Self; Astellas, AstraZeneca, Boehringer Ingelheim GmbH, Janssen Pharmaceuticals, Inc., Novo Nordisk Inc., Sanofi, Eli Lilly and Company, Orexigen Therapeutics, Inc., Merck &amp; Co., Inc..

Effects of the SGLT2 inhibitor ipragliflozin on food intake, appetite-regulating hormones, and arteriovenous differences in postprandial glucose levels in type 2 diabetic rats.

The sodium-glucose cotransporter (SGLT) 2 inhibitor, ipragliflozin, improves not only hyperglycemia but also obesity in type 2 diabetic animals and patients; however, there have been concerns that it may also cause an increase in compensatory food intake. Appetite is regulated by complex mechanisms involving the central nervous system, part of which involves appetite-related hormones and arteriovenous differences in postprandial glucose levels. We evaluated the effect of ipragliflozin in type 2 diabetic rats on food intake, appetite-related hormones and arteriovenous differences in postprandial glucose levels, and their correlation with food intake. Ipragliflozin and several antidiabetic drugs were administered to type 2 diabetic rats and various parameters concerning food intake were measured. Ipragliflozin significantly increased urinary glucose excretion and reduced postprandial hyperglycemia. Compared to normal rats, diabetic rats exhibited hyperphagia and elevated plasma levels of the appetite-stimulating hormones neuropeptide Y and ghrelin. Ipragliflozin induced significant weight loss and reduced plasma levels of appetite-stimulating hormones without affecting food intake. Diabetic rats exhibited a significantly reduced arteriovenous difference in postprandial glucose levels due to insulin insufficiency; this was improved by ipragliflozin, which increased renal arteriovenous differences in glucose levels by increasing urinary glucose excretion. These results indicate that the SGLT2 inhibitor, ipragliflozin, exerts antihyperglycemic actions by increasing urinary glucose excretion, and induces weight loss without a compensatory increase in food intake in type 2 diabetic mice. The mechanisms underlying these effects can be attributed, in part, to an increased arteriovenous difference in postprandial glucose levels and improved regulation of appetite-related hormones in the diabetic animal model. While this study was conducted in rodents and the results may be distinct from those in humans, it is possible that some of the pharmacological mechanisms, including the regulation of appetite-related hormones, can be extrapolated to clinical settings and may be valuable for further studies including clinical investigations.

Obese Mice Are Protected From Increased Energy Intake in Response to Voluntary Wheel Running

Diseases of metabolism pose an increasing threat to public health that has led to greater demand for effective treatments. Obesity is a highly prevalent metabolic disease that afflicts over 100 million Americans and increases the risk of developing diabetes and cardiovascular disease. Lifestyle modifications that incorporate exercise are a standard prescription for obesity, but its effectiveness is limited due to variability in compliance and physiological adaptations (e.g. compensatory increases in energy intake). Previous studies have shown that voluntary exercise fails to induce weight loss in high fat fed mice, but little is known regarding the onset of exercise. Here, we tested the hypothesis that chronic overnutrition from high fat feeding will mitigate the compensatory increase in food intake that commonly accompanies increased energy expenditure from voluntary exercise.Starting at 12 weeks of age, male C57BL/6J mice were weight matched, singly housed and fed a chow (n=8) or high fat diet (HFD; 60% calories from fat; n=6) for 4 weeks. At 18 weeks of age, mice were housed in a Promethion Metabolic Analyzer to measure energy expenditure, food intake and physical activity. Experiments were performed at 21°C with running wheels locked for four days then unlocked for the subsequent nine days. Body composition was assessed both prior to and immediately following indirect calorimetry experiments. Ethoscan (Sable Systems) analysis was performed to examine voluntary wheel running (VWR) distance, duration and speed and measured the time and distance for off‐wheel activities (i.e. roaming and feeding).HF‐fed mice were heavier (WT: 26.9 ± 1.1 vs. HF: 36.8 ± 4.2 g; p &lt; 0.05) and had greater fat mass (WT: 3.5 ± 0.6 vs. HF: 11.1 ± 3.1 g; p &lt; 0.05) than chow‐fed mice prior to energy balance studies. VWR caused a decrease in whole body (WT: −0.3 ± 0.8 vs. HF: −4.0 ± 1.3 g; p &gt; 0.05) and fat mass (WT: 0.3 ± 0.6 vs. HF: −3.0 ± 0.9 g; p &lt; 0.05) in HFD‐fed, but not in chow‐fed mice. VWR distance, duration, and speed were not affected by diet. VWR increased energy expenditure (EE) with both diets equally, but energy intake (EI) only increased in chow‐fed mice. VWR decreased overall off‐wheel activity (OWA) regardless of diet.These data demonstrate that 9 days of VWR cause weight loss in HFD‐fed mice but not mice fed a chow‐diet. Because VWR did not vary between diets, the efficacy of VWR in HFD‐fed mice could instead be attributed to resistance to specific behavioral compensations (i.e. increased food intake) that occur with the introduction of VWR in lean mice.Support or Funding InformationDSL (16POST29910001); D.H.W. (NIH DK054902 and DK076169)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Hypothalamic over-expression of VGF in the Siberian hamster increases energy expenditure and reduces body weight gain.

VGF (non-acronymic) was first highlighted to have a role in energy homeostasis through experiments involving dietary manipulation in mice. Fasting increased VGF mRNA in the Arc and levels were subsequently reduced upon refeeding. This anabolic role for VGF was supported by observations in a VGF null (VGF-/-) mouse and in the diet-induced and gold-thioglucose obese mice. However, this anabolic role for VGF has not been supported by a number of subsequent studies investigating the physiological effects of VGF-derived peptides. Intracerebroventricular (ICV) infusion of TLQP-21 increased resting energy expenditure and rectal temperature in mice and protected against diet-induced obesity. Similarly, ICV infusion of TLQP-21 into Siberian hamsters significantly reduced body weight, but this was due to a decrease in food intake, with no effect on energy expenditure. Subsequently NERP-2 was shown to increase food intake in rats via the orexin system, suggesting opposing roles for these VGF-derived peptides. Thus to further elucidate the role of hypothalamic VGF in the regulation of energy homeostasis we utilised a recombinant adeno-associated viral vector to over-express VGF in adult male Siberian hamsters, thus avoiding any developmental effects or associated functional compensation. Initially, hypothalamic over-expression of VGF in adult Siberian hamsters produced no effect on metabolic parameters, but by 12 weeks post-infusion hamsters had increased oxygen consumption and a tendency to increased carbon dioxide production; this attenuated body weight gain, reduced interscapular white adipose tissue and resulted in a compensatory increase in food intake. These observed changes in energy expenditure and food intake were associated with an increase in the hypothalamic contents of the VGF-derived peptides AQEE, TLQP and NERP-2. The complex phenotype of the VGF-/- mice is a likely consequence of global ablation of the gene and its derived peptides during development, as well as in the adult.

Review on Exercise Intervention Methods for Weight Loss in Obese Individuals

PURPOSE The prevalence of obesity in South Korea has been greatly increased over the past decades despite increases in one’s participation in weight reduction programs including exercise intervention. While it has been repeatedly shown that exercise has positive impacts on many health outcomes including lean body mass, fat mass, and insulin sensitivity, its effect on weight reduction is largely unclear. The purpose of this review was to summarize available data on the effect of exercise intervention on weight reduction and provide guidelines for developing effective exercise intervention, applicable to clinical practice. METHODS In this review, we reviewed currently available data mainly from meta-analytic studies and other available literature on the effect of therapeutic exercise intervention on weight loss. RESULTS Studies have generally shown that exercise intervention alone may not be effective in weight reduction due in part to insufficient exercise volume, compensatory increases in food intake, and so on. CONCLUSIONS It seems that exercise, especially when combined with other interventions such as diet, may enhance effectiveness of the weight loss intervention through increases in lean body mass and/or decreases in fat mass in an exercise volume dependent manner. 색인어: 비만, 운동량, 운동강도, ìš´ë™ì¢ ë¥˜, 체중감량 Keywords: Obesity, Exercise volume, Exercise intensity, Exercise type, Weight loss

Jodina rhombifolia leaves lyophilized aqueous extract decreases ethanol intake and preference in adolescent male Wistar rats

The leaves of Jodina rhombifolia (Hook. & Arn.) Reissek (Santalaceae) are utilized as anti-alcoholic in Argentine folk medicine. This study was designed to investigate the anti-alcohol properties in adolescent male Wistar rats (postnatal day 29; 83–105g of weight). We utilized the “self-administration model”, which ethanol was offered in the standard home-cage through two-bottle free-choice regimen between an ethanolic solution (20% in tap water, v/v) and tap water with unlimited access for 24h per day for 10 consecutive days. The results obtained show that repeated administration of J. rhombifolia lyophilized extract, markedly reduced ethanol voluntary intake on dose dependent bases. The magnitude in reduction of daily ethanol intake was approximately 29%, 44% and 68%, for the rat groups treated with 62.5, 125 and 250mg/kg of extract, respectively. Ethanol preference (proportion of ethanol intake versus total fluid intake) was significantly reduced: 21.37%±0.79 (0mg/kg); 15.83%±0.93 (62.5mg/kg); 15.22%±1.30 (125mg/kg) and 9.38%±0.57 (250mg/kg). Daily food intake was significantly higher (p<0.05) in the group treated with 250mg/kg of JRLE in comparison with vehicle-dose group; the reduction in ethanol intake was associated with a compensatory increase in food intake, probably because in the control group animals a part of the total caloric intake was supplied by ethanol. Treatment was very well tolerated by all animals and without apparent side-effects. These results contribute to the scientific validation of the antialcoholic indication of this botanic species in Argentine folk medicine.

Temperature matters with rodent metabolic studies.

An illusory goal in obesity therapeutics is to increase energy expenditure without provoking a compensatory rise in food intake. With the (re)discovery that functional and inducible brown fat exists in adult humans, studies aimed at understanding the physiology and activation of brown adipose tissue (BAT) have proliferated. Yet, intermittent cold exposure alone is often accompanied with an increase in food intake. Cold and β-adrenergic specific agonist treatments have both been shown to activate brown fat in adult humans, suggesting the feasibility of therapeutic activation of this tissue. Accordingly, Xiao et al. tested the physiologic and metabolic effects of a one-month subcutaneous infusion of {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243, a specific β3 adrenergic agonist that activates lipolysis in white adipose tissue and heat generation in brown adipose tissue. The authors tested this thermogenic molecule in mice fed standard chow and a high fat diet, housed at normal ambient housing temperatures (22°C) as well as at thermoneutrality (30°C). The authors found – as expected – that housing mice at thermoneutrality (30°) was associated with increased deposition of adipose tissue, impaired insulin sensitivity and a deactivation of BAT when compared to control mice housed at 22°C. At 22°C ambient, the {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243-treated mice maintained body weights similar to saline-treated animals by a compensatory increase in food intake whereas at 30°C ambient, {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243-treated mice lost body fat due to uncompensated (by food intake) increases in metabolic rate. These effects of ambient temperature on what constitutes therapeutic efficacy of {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243 are important. Although cogent arguments have been made for using thermoneutral housing conditions to test metabolic parameters in rodents[1], very few groups do so[2]. Rodent studies at both ambient room temperature and thermoneutrality have – not surprisingly – often shown opposite results. For example, Ucp1-/- mice are resistant to diet-induced obesity (DIO) at 22°C [3] but highly susceptible to the same diet when housed at 30°C [4], a reflection of the greater (∼40% higher) thermogenic stress imposed at 22°C. Likewise, mice lacking type 2 deiodinase (DioII-/-), a protein involved in the conversion of T4 to T3 in BAT and other tissues, are susceptible to DIO at 30°C but not at 22°C [5]. The same group tested 2-4 dinitrophenol (DNP) – another molecule capable of uncoupling oxidative phosphorylation, thereby producing heat – in mice at both ambient 22C and 30C temperatures and observed discordant phenotypes. Thus, ambient temperature clearly affects phenotypes related to energy homeostasis in rodents [1]. By virtue of their clothing and room thermostats, humans generally live at near thermoneutrality. Rodent housing at 22 degrees is comfortable for personnel, but imposes a major thermal stress on rodents – the degree depending upon airflow rates and numbers of animals per cage. If relevance to human physiology or therapeutics is a concern, housing at thermoneutrality (∼30°C for rodents) is likely to be important. Xiao would have missed the uncompensated (by food intake) increase in metabolic rate in animals treated with {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243 if the experiments had been conducted only at 22 degrees, because at the lower ambient extant metabolic stress masked the metabolic increment that {type:entrez-nucleotide,attrs:{text:CL316243,term_id:44896132,term_text:CL316243}}CL316243 delivers in animals housed at thermoneutrality.

Nutrient-specific feeding and endocrine effects of jejunal infusions in obese animals

Intestinal nutrient infusions result in variable decreases in food intake and body weight based on the nutrient type and the specific intestinal infusion site. We previously found that intrajejunal infusions of a fatty acid and glucose, but not casein hydrolysate, decreases food intake and body weight in lean chow-fed laboratory rats. To test whether obese, high fat-fed animals would show similar decreases in food intake and body weight in response to intrajejunal infusions of the same nutrients, equal kilocalorie loads of these nutrients (11.4 kcal) or vehicle were infused into the jejunum of obese, high fat-fed male Sprague-Dawley rats over 7 h/day for 5 consecutive days. Food intake was continuously monitored, and body weight was measured daily. After the infusion on the final day, rats were killed and plasma was collected. Similar to lean chow-fed rats, intrajejunal infusions of linoleic acid (LA) and glucose (Glu), but not casein hydrolysate (Cas), suppressed food intake with no compensatory increase in food intake after the infusion period. In contrast to lean chow-fed rats, only the LA, and not the Glu or Cas, produced decreases in body weight in the obese high fat-fed rat. There also were no differences in plasma glucagon-like peptide-1 levels in any of the nutrient infusion groups compared with saline infusion. These results suggest that there is a differential response to the same nutrients in lean vs. obese animals.

Effects of fasting and re-feeding on energy metabolism and thermogenesis in the tree shrew (Tupaia belangeri)

To investigate the effect of fasting and re-feeding on energy metabolism and thermogenesis in the tree shrew (Tupaia belangeri), the changes in body mass and body fat mass, resting metabolic rate (RMR), non-shivering thermogenesis (NST), body composition, mitochondrial cytochrome c oxidase (COX) activity in liver and brown adipose tissue (BAT), uncoupling protein-1 (UCP1) content of BAT, serum leptin level and post-fasting food intake were monitored and measured. The results showed that fasting induced a significant reduction in body mass and body fat mass. Body mass was restored to the control level in re-feeding tree shrew except for the body fat. RMR and NST decreased significantly in response to fasting, and returned to the control level after re-feeding. Fasting induced significant reduction in total, but not specific, COX activity (nmol O2/min/total tissue) in liver and BAT, and UCP1 content in BAT, which was reversed after re-feeding 48 h. Fasting of 12 h induced a rapid reduction in serum leptin content. There were no post-fasting compensatory increases in food intake. Interestingly, the tree shrew did not recover adipose tissue mass, nor serum leptin levels, upon re-feeding. These results suggest that T. belangeri can adjust the status of its physiology integratively to cope with the lack of food by means of decreasing body mass, adaptive thermogenesis and serum leptin levels, and serum leptin level acted as a starvation signal to mediate predominantly the reduction in body mass and energy expenditure.

How dieting makes some fatter: from a perspective of human body composition autoregulation

Dieting makes you fat - the title of a book published in 1983 - embodies the notion that dieting to control body weight predisposes the individual to acquire even more body fat. While this notion is controversial, its debate underscores the large gap that exists in our understanding of basic physiological laws that govern the regulation of human body composition. A striking example is the key role attributed to adipokines as feedback signals between adipose tissue depletion and compensatory increases in food intake. Yet, the relative importance of fat depletion per se as a determinant of post-dieting hyperphagia is unknown. On the other hand, the question of whether the depletion of lean tissues can provide feedback signals on the hunger-appetite drive is rarely invoked, despite evidence that food intake during growth is dominated by the impetus for lean tissue deposition, amidst proposals for the existence of protein-static mechanisms for the regulation of growth and maintenance of lean body mass. In fact, a feedback loop between fat depletion and food intake cannot explain why human subjects recovering from starvation continue to overeat well after body fat has been restored to pre-starvation values, thereby contributing to 'fat overshooting'. In addressing the plausibility and mechanistic basis by which dieting may predispose to increased fatness, this paper integrates the results derived from re-analysis of classic longitudinal studies of human starvation and refeeding. These suggest that feedback signals from both fat and lean tissues contribute to recovering body weight through effects on energy intake and thermogenesis, and that a faster rate of fat recovery relative to lean tissue recovery is a central outcome of body composition autoregulation that drives fat overshooting. A main implication of these findings is that the risk of becoming fatter in response to dieting is greater in lean than in obese individuals.

Nutrient Specific Feeding and Endocrine Effects of Jejunal Infusions

Intestinal nutrient infusions result in variable decreases in food intake and body weight based on the nutrient type and the specific intestinal infusion site. Only intrajejunal infusions of fatty acids decrease food intake beyond the calories infused. To test whether this extra-compensatory decrease in food intake is specific to fatty acids, small volume intrajejunal infusions of glucose (Glu) and casein hydrolysate (Cas), as well as linoleic acid (LA) were administered to male Sprague-Dawley rats. Equal kilocalorie (kcal) loads of these nutrients (11.4) or vehicle were infused into the jejunum over 7 h/day for five consecutive days. Food intake was continuously monitored and body weight was measured daily. After the infusion on the final day, rats were killed and plasma collected. Intrajejunal infusions of LA and Glu, but not Cas, suppressed food intake beyond the caloric load of the infusate with no compensatory increase in food intake after the infusion period. Rats receiving LA and Glu infusions also lost significant body weight across the infusion days. Plasma glucagon-like peptide-1 (GLP-1) was increased in both the LA and Glu rats compared with control animals, with no significant change in the Cas-infused animals. Peptide YY (PYY) levels increased in response to LA and Cas infusions. These results suggest that intrajejunal infusions of LA and Glu may decrease food intake and body weight via alterations in GLP-1 signaling. Thus, particular nutrients are more effective at producing decreases in food intake, body weight, and inducing changes in peptide levels and could lead to a novel therapy for obesity.

Effect of a 3-day high-fat feeding period on carbohydrate balance and ad libitum energy intake in humans

A reduction in glycogen after the switch to an isoenergetic high-fat diet (HFD) might promote a compensatory increase in food intake to reestablish carbohydrate balance. We assessed the effect of an isoenergetic switch from a 49%-carbohydrate to 50%-fat diet on nutrient balance and ad libitum food intake. We hypothesized that carbohydrate balance would be inversely related to ad libitum energy intake. In 47 men and 11 women (22.6+/-0.4 years; 26.1+/-0.5 kg m(-2)), fuel balance was measured in a respiration chamber over 4 days. During the first day, an isoenergetic, high-carbohydrate diet was provided followed by a 3-day isoenergetic, HFD. At the end of this period and after 16 h of fasting, three options of foods (cookies, fruit salad and turkey sandwich) were offered ad libitum for 4 h. The relationships between post-chamber ad libitum intake and macronutrient oxidation and balance measured day-to-day and over the 4-day respiration chamber stay were studied. After switching to a HFD, 24-h respiratory quotient decreased from 0.87+/-0.02 to 0.83+/-0.02 (P<0.0001) resulting in a 4-day cumulative carbohydrate, fat and protein balances of -183+/-368, 342+/-480 and 65+/-267 kcal, respectively. Cumulative energy balance (224+/-362 kcal per 4 days) did not influence ad libitum energy intake. However, we detected that 4-day carbohydrate balance was a positive and independent predictor of post-chamber ad libitum energy intake (R (2)=0.10; P=0.01), whereas no significant influence of fat and protein balances was found. In response to an isoenergetic change from a high-carbohydrate to HFD, higher carbohydrate balance related to increased energy intake.

Effects of fasting and refeeding on body mass, thermogenesis and serum leptin in Brandt's voles ( Lasiopodomys brandtii)

(1) To investigate the effect of fasting and refeeding on the body mass, thermogenesis and serum leptin in Brandt's voles, the changes in body and body fat mass, resting metabolic rate (RMR), mitochondrial cytochrome c oxidase (COX) activity in liver and brown adipose tissue (BAT), uncoupling protein 1 (UCP1) content of BAT, serum leptin level and post-fasting food intake were monitored and measured. (2) Fasting induced significant reduction in body mass and body fat mass. Body mass can be restored to the control level in refeeding voles except for the body fat. (3) RMR decreased significantly in response to fasting, and can return to the control level after refeeding. Fasting induced significant reduction in total, but not specific, COX activity (nmol O 2/min/total tissue) in liver and BAT, and UCP1 content in BAT, which was reversed after refeeding of 48 h. (4) Fasting for 12 h induced a rapid reduction in serum leptin content. There were no post-fasting compensatory increases in food intake. Interestingly, Brandt's voles did not recover adipose tissue mass, nor serum leptin levels, on refeeding. (5) Our data indicate that Brandt's voles can adjust their physiological functions integratively to cope with the starvation by the means of decreasing body mass, adaptive thermogenesis and serum leptin levels. There is no post-fasting hyperphagia in Brandt's voles. The reduction of serum leptin was somewhat earlier than the decline in body fat and body mass.

Catecholamine Reuptake Inhibition Causes Weight Loss by Increasing Locomotor Activity and Thermogenesis

Bupropion (BUP) is a dopamine (DA) and norepinephrine (NE) reuptake inhibitor that causes mild weight loss in obese adults. Subchronic (7 day) coadministration of selective DA and NE reuptake inhibitors also causes weight loss in mice. Because weight loss was not associated with decreased caloric intake, subchronic BUP might cause weight loss through increased energy expenditure. Acute studies demonstrate that BUP or DA+NE reuptake inhibitors cause transient hypophagia and increased locomotion; though the effects on temperature are inconsistent. Because subchronic DA+NE reuptake inhibition does not affect appetite, there is clearly a difference between the acute and subchronic effects of DA+NE reuptake inhibitors; however the effects of chronic (or subchronic) BUP on energy balance have never been directly studied in an animal model. Therefore, the acute and subchronic effects of BUP or selective DA and NE reuptake inhibitors on food intake, body weight, locomotor activity, and interscapular temperature were determined in mice. Generally, selective inhibition of DA reuptake (by GBR12783) increased activity while selective inhibition of NE reuptake (by nisoxetine, NIS) decreased activity and temperature. BUP increased activity and temperature but subchronic BUP did not significantly reduce body weight due to a compensatory increase in food intake. Subchronic DA+NE reuptake inhibitor coadministration mimicked the effect of BUP on activity and temperature, but caused weight loss because daily food intake was not increased. The results of this study suggest that the mild weight loss effect of BUP in humans may be due to increased locomotion or heat production. More importantly, inhibition of DA+NE reuptake (with GBR+NIS) increased energy expenditure without a compensatory increase in food intake, supporting a role for novel combination catecholamine reuptake inhibitors in pharmacotherapy for obesity.

Food hoarding is increased by food deprivation and decreased by leptin treatment in Syrian hamsters.

Compensatory increases in food intake are commonly observed after a period of food deprivation in many species, including laboratory rats and mice. Thus it is interesting that Syrian hamsters fail to increase food intake after a period of food deprivation, despite a fall in plasma leptin concentrations similar to those seen in food-deprived rats and mice. In previous laboratory studies, food-deprived Syrian hamsters increased the amount of food hoarded. We hypothesized that leptin treatment during food deprivation would attenuate food-deprivation-induced increases in hoarding. Baseline levels of hoarding were bimodally distributed, with no hamsters showing intermediate levels of hoarding. Both high (HH) and low hoarding (LH) hamsters were included in each experimental group. Fifty-six male hamsters were either food deprived or given ad libitum access to food for 48 h. One-half of each group received intraperitoneal injections of leptin (4 mg/kg) or vehicle every 12 h during the food-deprivation period. Within the HH group, the hoarding score increased significantly in food-deprived but not fed hamsters (P < 0.05). Leptin treatment significantly decreased hoarding in the food-deprived HH hamsters (P < 0.05). The LH hamsters did not increase hoarding regardless of whether they were food deprived or had ad libitum access to food. These results are consistent with the idea that HH hamsters respond to energetic challenges at least in part by changing their hoarding behavior and that leptin might be one factor that mediates this response.

Feeding dynamics in fish experiencing cycles of feed deprivation: a comparison of four species

Abstract The temporal dynamics of daily food consumption were examined in individually housed fish that experienced four cycles of 1 week of feed deprivation followed by 2 weeks of feeding to satiation. Four species were compared: European minnows Phoxinus phoxinus: Cyprinidae; three-spined sticklebacks Gasteosteus aculeatus: Gasterosteidae: gibel carp Carassius auratus gibelio: Cyprinidae; and the longsnout catfish Leiocassis longirostris: Bagridae. The stickleback, carp and catfish showed significant compensatory increases in food intake following deprivation, with the response becoming clearer in successive cycles. The temporal pattern of consumption during the refeeding periods differed between the four species. In sticklebacks, daily intake over a refeeding period initially decreased, but then recovered. In minnows, intake tended to decline over a refeeding period. Gibel carp showed an increase in daily intake on refeeding, but this may have reflected an adverse response to weighing. Over a refeeding period, catfish had a weak tendency to show an initial decline, followed by an increase. These differences are discussed in relation to differences in experimental protocols and biological differences between the species.

Physical activity and regulation of food intake: current evidence.

The evidence was reviewed on how physical activity could influence the regulation of food intake by either adjusting the sensitivity of appetite control mechanisms or by generating an energy deficit that could adjust the drive to eat. Interventionist and correlational studies that had a significant influence on the relationship between physical activity and food intake were reviewed. Interventionist studies involve a deliberate imposition of physical activity with subsequent monitoring of the eating response. Correlational studies make use of naturally occurring differences in the levels of physical activity (between and within subjects) with simultaneous assessment of energy expenditure and intake. Studies using lean, overweight, and obese men and women were included. Only 19% of interventionist studies report an increase in energy intake after exercise; 65% show no change and 16% show a decrease in appetite. Of the correlational studies, approximately half show no relationship between energy expenditure and intake. These data indicate a rather loose coupling between energy expenditure and intake. A common sense view is that exercise is futile as a form of weight control because the energy deficit drives a compensatory increase in food intake. However, evidence shows that this is not generally true. One positive aspect of this is that raising energy expenditure through physical activity (or maintaining an active life style) can cause weight loss or prevent weight gain. A negative feature is that when people become sedentary after a period of high activity, food intake is not "down-regulated" to balance a reduced energy expenditure. Evidence suggests that a high level of physical activity can aid weight control either by improving the matching of food intake to energy expenditure (regulation) or by raising expenditure so that it is difficult for people to eat themselves into a positive energy balance.

Physical activity in the prevention and treatment of obesity and its comorbidities: evidence report of independent panel to assess the role of physical activity in the treatment of obesity and its comorbidities.

Physical activity in the prevention and treatment of obesity and its comorbidities: evidence report of independent panel to assess the role of physical activity in the treatment of obesity and its comorbidities.

Peroxisome proliferators as adjuvants for the reverse-electron-transport therapy of obesity: an explanation for the large increase in metabolic rate of MEDICA 16-treated rats

The efficacy of reverse-electron-transport therapy of obesity should be promoted by agents which up-regulate hepatocyte enzymes that are potentially rate-limiting for mitochondrial fatty acid oxidation and electron shuttles. Peroxisome proliferator drugs, including the fibrates used to treat hyperlipidemia, may be useful in this regard, as they induce malic enzyme, the mitochondrial glycerol-3-phosphate dehydrogenase, and carnitine palmitoyl transferase I in rodent hepatocytes. An agent of this class, MEDICA 16, has the additional property of potently inhibiting both citrate lyase and acetyl-CoA carboxylase. As a result, me thyl-substituted di a ca rboxylic acids (MEDICA) 16 can be expected to disinhibit hepatic fatty acid oxidation while up-regulating electron shuttle mechanisms, and thus should stimulate reverse electron transport. This may explain the remarkable 40% increase in basal metabolic rate observed in normal rats ingesting MEDICA 16 – an effect not associated with any compensatory increase in food intake. Relative to controls, the MEDICA 16-treated rats achieved a 50% reduction in body fat and a modest increase in lean mass, such that weight and growth were not changed. In other rodent strains, MEDICA 16 has prevented obesity diabetes and atherogenesis. However, whether MEDICA 16 and other peroxisome proliferator drugs will have clinical utility in reverse-electron-transport therapy may hinge on their ability to induce key enzymes inhuman hepatocytes; cell culture studies to evaluate this are required.