Regulation Of Energy Intake Research Articles

The impact of intronic single nucleotide polymorphisms and ethnic diversity for studies on the obesity gene FTO

In 2007, the first common genetic variants were identified, which undoubtedly affect our susceptibility to obesity. These variants are located in the fat mass and obesity-associated gene FTO. Since then, over 50 loci for common obesity have been identified. As the research on these loci is still at an early stage, there is a great need to review, for clarification purposes, the current research on FTO, as this is likely to influence future studies. Based on the current knowledge, FTO seems to be directly involved in the regulation of energy intake, but there is an urgent need for the identification of regulatory polymorphisms. Thus, herein, we discuss current knowledge and highlight putative functional regions in FTO based on published data and computer-based analysis.

Obesidad monogénica humana: papel del sistema leptina-melanocortina en la regulación de la ingesta de alimentos y el peso corporal en humanos

Human obesity is a disorder of multifactorial origin in which genetic and environmental factors are involved. To understand the mechanisms regulating energy intake and fat accumulation in the body, it is important to study the genetic alterations causing monogenic obesity. Most of the genes involved in monogenic obesity are associated with the leptin-melanocortin system; hence the importance of studying this system by analysing natural mutations in mice. Previous studies have described mutations in leptin and its receptor, proopiomelanocortin and prohormone convertase 1 associated with human obesity of monogenic origin. The aim of this study is to provide an updated review of the main characteristics and functioning of the leptin-melanocortin system, and its implications and potentialities in regulating food intake and body weight.

Discussion of “Overweight and obese boys reduce food intake in response to a glucose drink but fail to increase intake in response to exercise of short duration”

Tamam and collaborators recently proposed an interesting paper addressing the food intake and appetite response to an acute exercise and a glucose drink in normal weight and overweight–obese adolescents (Tamam et al. 2012). This paper adds great and useful results to the actual literature but to our mind some issues have to be underlined. The authors state that their paper is the first to provide data regarding the impact of acute effect of short exercise on energy intake in 9to 14-year-old boys while previous recent studies have explored the impact of three 10-min bouts of exercise (Thivel et al. 2011a, 2011b, 2012b). In this paper, overweight–obese adolescent boys do not modify their energy intake after a 15min bout of exercise set at their ventilatory threshold, whereas it has been shown that acute intensive exercise (>70% maximal oxygen consumption) was able to induce a decrease energy intake in such a population at the following ad libitum meal (Thivel et al. 2011a, 2011b, 2012b). The important exercise-induced energy expenditure differences between those last studies (about 300 kcal) and the present one (63 ± 7 kcal) may explain such a discrepancy, but we recently suggested that the energy expended during exercise does not explain the subsequent energy consumption since food intake was differentially affected after isoenergetic exercises at 2 levels of intensity (40% and 75% maximal oxygen consumption) (for review see Thivel et al. 2012a, 2012b). To our view the main reasons that Tamam et al. did not find any differences are the short duration of the follow-up, dinner energy intake was not examined, and most importantly, the use of ad libitum pizza buffets that are highly palatable and could have favoured inconsistent energy intake in those youths. In our previous work, we chose buffet meals composed of a high diversity of food without the participant’s preferred items to avoid the hedonic influence on food intake. The “non-homeostatic” regulation of energy intake certainly overpasses the physiological pathways involved in presence of highly palatable items (Finlayson and Dalton 2012). An important decreased food intake at dinner time without appetite modification (about 7 h after the exercise session) has also been reported by our group, whereas Tamam and colleagues suggested that the increased appetite sensation observed after exercise could favour higher energy consumption later in the day. Based on the already shown uncoupling effect of exercise on subjective appetite and effective energy consumption in both adults and youths (Flint et al. 2000; Mattes 1990; Thivel et al. 2011a, 2012b), it appears difficult to formulate such a hypothesis. Finally, the authors conclude that an acute short-term exercise set at the ventilator threshold was able to reduce energy balance because of energy expenditure and in the absence of subsequent energy intake compensation. However, the covered period in which to assess energy balance seems too short to hypothesize so (which was pointed out by the authors) as compensatory trends have been underlined in overweight– obese children who decrease their spontaneous energy expenditure after such an exercise for the rest of the day (Kriemler et al. 1999; Thivel et al. 2012a, 2012b). This compensatory response leads once more to the consideration of whether the best impact of physical activity for weight control and weight loss remains the induced energy expenditure or its impact on energy intake (Chaput and Sharma 2011). The paper proposed by Tamam and collaborators provides then interesting results concerning the impact of a glucose drink on food intake in lean and overweight–obese youths but the interpretation of their data on the energy in-

The Loss of Metabolic Control on Alcohol Drinking in Heavy Drinking Alcohol-Dependent Subjects

BackgroundMost physiological studies interested in alcohol-dependence examined ethanol as a pharmacological agent rather than a nutrient. We conducted two studies, which assessed the metabolic and endocrine factors involved in the regulation of alcohol and nutrient intake in alcohol-dependent (AD) subjects. We also examined the potential role of a disruption in energy balance in alcohol-dependence.Methods and ResultsIn Study-1, quantitative dietetic interviews of eating and drinking habits were conducted with 97 AD subjects. The population was split around a median alcohol intake value of 12.5 kcal/kg/day. The results showed that the “low alcohol” drinking AD subjects had high Body Mass Index (BMI) and Fat Mass (FM) and alcohol intake was compensated for by a decrease in non-alcoholic intakes. “High alcohol” drinking AD subjects, on the other hand, had low BMI and FM and the total caloric intakes were largely above norms. In Study-2, 24 AD inpatients were submitted to dietetic interviews, calorimetry and blood samplings for the measurement of biomarkers of the regulation of metabolism and satiety, on day 2, 5 and 16 of abstinence. These patients were compared with 20 controls matched for age and gender. We observed in AD patients an increase in cortisol, leptin and PYY plasma levels and a decrease in ghrelin, which might explain the observed decrease in non-alcoholic intakes. However, alcoholic and non-alcoholic intakes correlated positively with basal metabolism and negatively with leptin and leptin/BMI.ConclusionFor individuals consuming below12.5 kcal/kg/day of alcohol, alcohol intake is compensated for by a decrease in non-alcoholic nutrient intakes, probably due to changes in metabolic and satiety factors. For individuals consuming above 12.5 kcal/kg/day of alcohol, alcohol accelerates metabolism and decreases fat mass and leptin levels, and the total caloric intake largely exceeds norms. A dual model for regulation of energy intake in AD subjects is proposed.

Acute Exercise and Subsequent Nutritional Adaptations

The imbalance between energy expenditure and energy intake is the main factor accounting for the progression of obesity. For many years, physical activity has been part of weight-loss programmes to increase energy expenditure. It is now recognized that exercise can also affect appetite and energy consumption. In the context of seeking new obesity treatments, it is of major interest to clarify the impact of physical exercise on energy intake. Many reviews on this topic have been published regarding both lean and overweight adults, and this review focuses on the relationships between acute exercise and the short-term regulation of energy intake in lean and overweight or obese youths. The current literature provides very few data regarding the impact of exercise on subsequent energy intake and perceived and measured appetite in children and adolescents, mainly because of methodological difficulties in the assessment of both energy intake and expenditure. It has been long suggested that energy intake was regulated after exercise in order to compensate for the exercise-induced energy expenditure and then preserve energy balance. This overview underlines that the energy expended during exercise is not the main parameter that influences subsequent energy intake in both lean and overweight/obese children and adolescents, and that factors such as the duration or intensity of exercise may have larger impact. The effects of acute exercise on the following nutritional adaptations (energy intake and appetite feelings) remain inconclusive in lean youths, mainly due to the lack of data and the disparity of the methodologies used. Studies in overweight or obese children and adolescents are confronted with the same difficulties, and the few available data suggest that intensive exercise (>70% maximal oxygen consumption) can induce a reduction in daily energy balance, as a result of its anorexigenic effect in obese adolescents. However, further studies are needed to clarify the impact of acute exercise on subsequent nutritional adaptations and appetite-related hormones in children and adolescents, and to investigate the effect of chronic exercise programmes.

Neural and metabolic regulation of macronutrient intake and selection

There is considerable disagreement regarding what constitutes a healthy diet. Ever since the influential work of Cannon and Richter, it was debated whether the 'wisdom of the body' will automatically direct us to the foods we need for healthy lives or whether we must carefully learn to eat the right foods, particularly in an environment of plenty. Although it is clear that strong mechanisms have evolved to prevent consumption of foods that have previously made us sick, it is less clear whether reciprocal mechanisms exist that reinforce the consumption of healthy diets. Here, we review recent progress in providing behavioural evidence for the regulation of intake and selection of proteins, carbohydrates and fats. We examine new developments in sensory physiology enabling recognition of macronutrients both pre- and post-ingestively. Finally, we propose a general model for central neural processing of nutrient-specific appetites. We suggest that the same basic neural circuitry responsible for the homoeostatic regulation of total energy intake is also used to control consumption of specific macro- and micronutrients. Similar to salt appetite, specific appetites for other micro- and macronutrients may be encoded by unique molecular changes in the hypothalamus. Gratification of such specific appetites is then accomplished by engaging the brain motivational system to assign the highest reward prediction to exteroceptive cues previously associated with consuming the missing ingredient. A better understanding of these nutrient-specific neural processes could help design drugs and behavioural strategies that promote healthier eating.

Fiber intake Inconsistently Alters Gut Hormone Levels in Humans Following Acute or Chronic Intake

Diet composition affects the release of gut hormones involved in the regulation of appetite and energy intake. While some research suggests high fiber foods cause greater satiety than low fiber foods, few studies have measured gut hormone levels as a mechanism by which fiber may influence appetite. A review of the literature was conducted to better understand the effect of fiber on gut hormone concentrations in humans, which specific focus on peptide YY, glucagon-like peptide-1, cholecystokinin, and ghrelin. Considerable variation was found in study design, population, fiber type and level. Few studies reported a significant effect of fiber on gut hormone levels, and data suggest caloric load may have a more significant influence on gut hormone release. While it is possible that circulating gut hormones are not the mechanism by which fibers influence satiety, it is also possible that variability in study design prevents definitive conclusions around this relationship.

Infant regulation of intake: the effect of free glutamate content in infant formulas

We recently discovered that infants randomly assigned to a formula high in free amino acids (extensive protein hydrolysate formula; ePHF) during infancy consumed less formula to satiation and gained less weight than did infants fed an isocaloric formula low in free amino acids (cow milk formula; CMF). Because ePHF and CMF differ markedly in concentrations of free glutamate, we tested the hypothesis that the higher glutamate concentrations in ePHF promote satiation and satiety. In this counterbalanced, within-subject study, infants <4 mo of age (n = 30) visited our laboratory for 3 sets of 2 consecutive infant-led formula meals over 3 test days. Infants were fed 1 of 3 isocaloric formulas during each first meal: CMF, ePHF, or CMF with added free glutamate to approximate concentrations in ePHF (CMF+glu). When infants signaled hunger again, they were fed a second meal of CMF. From these data, we calculated satiety ratios for each of the 3 formulas by dividing the intermeal interval by the amount of formula consumed during that particular first meal. Infants consumed significantly less CMF+glu (P < 0.02) and ePHF (P < 0.04) than CMF during the first meals. They also showed greater levels of satiety after consuming CMF+glu or ePHF: satiety ratios for CMF+glu (P < 0.03) and ePHF (P < 0.05) were significantly higher than for CMF. These findings suggest a role of free glutamate in infant intake regulation and call into question the claim that formula feeding impairs infants' abilities to self regulate energy intake.

A review of dietary energy density and obesity

The role of dietary energy density (ED) in energy intake regulation and weight management remains controversial. Relationships between ED, energy intake and body weight were determined in a review of pertinent studies examining the effects of ED on energy intake (EI) and/or body weight in non‐elderly adults. Sixty‐nine relevant studies in which effects of ED could be separated from other putative determinants of energy regulation including dietary fiber were identified. Observational studies generally report positive associations between dietary ED and BMI, risk for overweight/obesity or weight gain. Short‐term clinical trials consistently demonstrate that decreasing preload, individual meal or 24‐h dietary ED results in a reduction in EI proportional to the magnitude of the reduction in ED. Longer‐term (&gt;1 mo) randomized clinical trials suggest that reducing the ED of diets consumed ad libitum may promote modest weight loss; however, based on very limited available studies, ED modification may have no additional weight loss benefit when recommended in conjunction with an energy restricted diet. In summary, a substantial body of evidence demonstrates that short‐term decreases in ED promote reductions in EI, but the extent to which low ED diets facilitate weight loss or prevent weight gain remains undetermined. Further studies are needed to elucidate the role of ED in long‐term weight management.Grant Funding Source: NA

Effects of Increased Dietary Protein at Breakfast on Appetite Control &amp; Energy Intake Throughout the Day in Overweight ‘Breakfast Skipping’ Teen Girls

PurposeTo examine whether a higher‐protein (HP) vs. normal‐protein (NP) breakfast leads to daily improvements in appetite control and energy intake regulation in overweight ‘breakfast skipping’ (BS) girls.MethodsTwenty girls (age 19 ±1 y; BMI 28.6 ± 0.7 kg/m2; BS 6 ± 1 x/wk) randomly consumed 350 kcal breakfast meals containing NP cereals (15% Protein (13 g); 65% CHO; 20% Fat) or HP, egg and beef‐based foods (40% Protein (35 g); 40% CHO; 20% Fat) for 7 consecutive days. On day 7 of each pattern, a 10 h testing day was completed. At the onset of the respective breakfast, perceived appetite/satiety questionnaires and blood sampling were completed every 30 min. A standard lunch occurred 4 h post‐breakfast; an ad libitum dinner was consumed 4 h post‐lunch, and ad libitum snacks were packed out to be consumed at home throughout the evening.ResultsThe HP breakfast led to greater increases in perceived satiety, reductions in ghrelin, and increases in PYY responses vs. NP (p&lt;0.05, all). HP breakfast also led to reduced snacking, particularly of foods high in fat vs. NP (energy content: 486 ± 84 vs. 621 ± 110 kcal; p=0.07; fat content: 17.4 ± 3.6 vs. 23.8 ± 4.4 g; p&lt;0.05).ConclusionsA higher protein breakfast meal containing 35 g of protein improved appetite control, satiety, and reduced unhealthy snacking in ‘breakfast skipping’ overweight teenage girls. Support: Beef Checkoff &amp; the American Egg Board/Egg Nutrition Center

Comparison of a higher protein yogurt vs. other commonly consumed afternoon snacks on time to meal request

PurposeTo determine whether an afternoon snack of higher‐protein yogurt, (14 g protein, HPY) delays the onset of eating vs. other commonly consumed eucaloric snacks varying in macronutrient content, including Pretzels (P), Crackers (Cr), Chocolate (Ch), and No Snack (NS).MethodsUsing a randomized crossover design, 23 women (age 27 ± 1y; BMI 23.4 ± 0.6) were acclimated to each snack for 3 consecutive days. On day 4, the participants consumed a standard breakfast, at home, and came to our facility 1 hr prior to their habitual lunch time. A standard lunch was provided followed by their respective snack (160 kcal) consumed 3 h post‐lunch. Subjective appetite was assessed by VAS completed every 30 min throughout the afternoon until dinner was voluntarily requested.ResultsNS led to an earlier dinner request time (2:09 ± 0:37 h) vs. HPY (2:43 ± 0:39 h; p&lt;0.001), P (2:40 ± 0:31 h, p&lt;0.001), and Cr (2:24 ± 0:38 h p=0.08), but not Ch (2:18 ± 0:39 h post‐snack). Between snacks, HPY and P had a greater delay in eating vs. Ch (p&lt;0.05, both); HPY also led to a greater delay vs. Cr (p=0.09).ConclusionsA higher‐protein afternoon yogurt snack delayed subsequent eating vs. crackers and chocolate while a pretzel snack delayed subsequent eating longer than chocolate, suggesting that macronutrient content and sensory characteristics of snacks influence energy intake regulation. Funded by: General Mills, Inc.

Gut bacteria profiles of Mus musculus at the phylum and family levels are influenced by saturation of dietary fatty acids

BackgroundMammalian gut microbiota have been implicated in a variety of functions including the breakdown of ingested nutrients, the regulation of energy intake and storage, the control of immune system development and activity, and the synthesis of novel chemicals. Previous studies have shown that feeding mammalian hosts a high-fat diet shifts gut bacteria at the phylum level to reduce the ratio of Bacteroidetes-to-Firmicutes, while feeding hosts a fat-restricted diet increases this ratio. However, few studies have investigated the differential effects of fatty acid type on gut bacterial profile. MethodsOver a 14-week period, Mus musculus were fed a diet rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs), omega-6 polyunsaturated fatty acids (n-6 PUFAs), or saturated fatty acids (SFAs). Fecal pellets were collected before and after the treatment period from 12 randomly selected mice (4 per treatment group). Bacterial DNA was extracted from the pellets and characterized by analysis of the hypervariable V3 region of the 16S rRNA. Nominal logistic regression models were used to assess shifts in microbial profile at the phylum and family levels in response to diet. ResultsA significant decrease in the proportion of phylum Bacteroidetes species was observed for mice fed any of the three diets over time. However, the SFA-rich diet group showed a significantly greater decrease in Bacteroidetes proportion (−28%) than did either the n-3 PUFA group (−10%) or the n-6 PUFA group (−12%). At the family level, a significant decrease in proportion of Porphyromonadaceae was observed for mice fed the n-6 PUFA-rich diet, and a significant decrease in proportion of Lachnospiraceae was observed for mice fed the SFA-rich diet. There was no significant effect of diet type on body mass change. ConclusionOur results indicate that SFAs have stronger effects than PUFAs in shifting gut microbiota profiles toward those typical of obese individuals, and that dietary fatty acid saturation influences shifts in gut microbiota independently of changes in body mass.

Associations between eating patterns, dietary intakes and eating behaviors in premenopausal overweight women

The regulation of energy intake is complex and many biological, psychosocial and environmental influences have been identified. To our knowledge, no study has yet investigated how eating patterns could mediate associations between eating behaviors and self-reported energy intake in premenopausal overweight women. Therefore, objectives of this study were to examine associations between eating behaviors and eating patterns in premenopausal overweight women and to test if eating patterns could mediate the associations between eating behaviors and self-reported energy intake. Women completed a 3-day food record and the Three-Factor Eating Questionnaire was used to assess eating behaviors (dietary restraint, disinhibition, hunger). In the total sample of women, flexible restraint was negatively (r=−0.18; p=0.03) and binge eating severity was positively (r=0.24; p=0.004) associated with self-reported energy intake. Moreover, flexible restraint was positively associated with the proportion of energy intake at breakfast (r=0.24; p=0.004), whereas disinhibition and binge eating severity were positively associated with the proportion of energy intake from snacks consumed after 5:00 pm (r=0.22, p=0.007 and r=0.22, p=0.01, respectively). In addition, mediational analyses showed that proportion of energy intake from snacks consumed after 5:00 pm explained 24.1% of the association between binge eating severity and self-reported energy intake. In conclusion, these results suggest that eating patterns are important factors to consider in order to explain the associations between eating behaviors and self-reported energy intake.

Colonic flora, Probiotics, Obesity and Diabetes

Obesity results from alterations in the body’s regulation of energy intake, expenditure, and storage. Animal and human data demonstrate that phylogenic changes occur in the microbiota composition in obese individuals. Furthermore, evidence from animal models suggest that the alterations of the gut microbiota with obesity results in increased energy extraction and lipid deposition, altered release of entero-hormones, increased intestinal permeability and metabolic endotoxemia. Treatment with pre- and probiotics may reverse many of metabolic effects linked with the altered microbiota in obese patients. The gut microbiota is, therefore, a potential nutritional and pharmacological target for the management of obesity and obesity-related disorders.

Parental Influences on Children's Self-Regulation of Energy Intake: Insights from Developmental Literature on Emotion Regulation

The following article examines the role of parents in the development of children's self-regulation of energy intake. Various paths of parental influence are offered based on the literature on parental influences on children's emotion self-regulation. The parental paths include modeling, responses to children's behavior, assistance in helping children self-regulate, and motivating children through rewards and punishments. Additionally, sources of variation in parental influences on regulation are examined, including parenting style, child temperament, and child-parent attachment security. Parallels in the nature of parents' role in socializing children's regulation of emotions and energy intake are examined. Implications for future research are discussed.

Altered Default Network Activity in Obesity

The regulation of energy intake is a complex process involving the integration of homeostatic signals and both internal and external sensory inputs. To better understand the neurobiology of this process and how it may be dysfunctional in obesity, this study examined activity of the brain's "default network" in reduced-obese (RO) as compared to lean individuals. The default network is a group of functionally connected brain regions thought to play an important role in internally directed cognitive activity and the interplay between external and internal sensory processing. Functional magnetic resonance imaging was performed in 24 lean and 18 RO individuals in the fasted state after 2 days of eucaloric energy intake and after 2 days of 30% overfeeding in a counterbalanced design. Scanning was performed while subjects passively viewed images of food and nonfood objects. Independent component analysis was used to identify the default network component. In the eucaloric state, greater default network activity was observed in RO compared to lean individuals in the lateral inferior parietal and posterior cingulate cortices. Activity was positively correlated with appetite. Overfeeding resulted in increased default network activity in lean but not RO individuals. These findings suggest that the function of the default network, a major contributor to intrinsic neuronal activity, is altered in obesity and/or obese-prone individuals. Future studies of the network's function and its relationship to other brain networks may improve our understanding of the mechanisms and treatment of obesity.

Developmental programming of adult obesity and cardiovascular disease in rodents by maternal nutrition imbalance

Studies on fetal undernutrition have generated the hypothesis that fetal programming corresponds to an attempt of the fetus to adapt to adverse conditions encountered in utero. These adaptations would be beneficial if these conditions prevail later in life, but they become detrimental in the case of normal or plentiful nutrition and favor the appearance of the metabolic syndrome. In this article, the discussion is limited to the developmental programming of obesity and cardiovascular disorders caused by an early mismatched nutrition, particularly intrauterine growth retardation followed by postnatal catch-up growth. Selected data in humans are reviewed before evoking some mechanisms revealed or suggested by experiments in rodents. A variety of physiologic mechanisms are implicated in obesity programming, 2 of which are detailed. In some, but not all observations, hyperphagia resulting namely from perturbed development of the hypothalamic circuitry devoted to appetite regulation may contribute to obesity. Another contribution may be the developmental changes in the population of fat cell precursors in adipose tissue. Even if the link between obesity and cardiovascular disease is well established, alteration of blood pressure regulation may appear independently of obesity. A loss of diurnal variation in heart rate and blood pressure in adulthood has resulted from maternal undernutrition followed by postnatal overnutrition. Further research should clarify the effect of mismatched early nutrition on the development of brain centers regulating energy intake, energy expenditure, and circadian rhythms.

Use of self-feeders to evaluate macronutrient self-selection and energy intake regulation in Nile tilapia

Our objective was to evaluate the capacity of Nile tilapia ( Oreochrmis niloticus) to self-select the most nutritious foods when offered with other foods. The fish were offered pairs of macronutrients (protein + carbohydrate, PC; protein + fat, PF; carbohydrate + fat, CF) in three self-feeders and subjected to different challenges: i) the relative position of the self-feeders was changed, ii) the protein content was reduced by 50%, and iii) protein was withdrawn. In the experiment, 90 males (142.0 ± 18.0 g) were kept in 6 tanks (150 l each) and their daily macronutrient intake was calculated. Regardless of the self-feeder position, fish composed a diet containing 41.7% P, 34.8% C and 23.5% F, and a relatively stable energy content of around 187.0 kJ/kg BW/day. When the protein-containing diets (PC and PF) were diluted by 50%, fish increased their food intake to compensate for the energy dilution and thus sustain the dietary composition (42.6% P, 33.3% C and 23.2% F). Finally, when PC and PF were removed, fish maintained the energy intake at around 178.2 kJ/kg BW/day. These results indicate that tilapia can adapt to protein dilution/removal to sustain its energy intake, making it a useful model for dietary selection and nutritional studies.

Serum Leptin, Energy Budget, and Thermogenesis in Striped Hamsters Exposed to Consecutive Decreases in Ambient Temperatures

Leptin has been found to be a direct participant in the regulation of both energy intake and energy expenditure in small mammals showing seasonal declines in body mass (M(b)) and fat mass, but its roles in an animal exhibiting seasonally increased thermogenesis and unchanged M(b) remain unclear. Serum leptin levels, energy budget, and thermogenesis were measured in striped hamsters exposed to consecutive decreases in ambient temperatures ranging from 23° to -23°C. Cold-exposed hamsters had significant increases in gross energy intake (GEI), the rate of basal metabolism, nonshivering thermogenesis, and activity of cytochrome c oxidase (COX) in brown adipose tissue (BAT), compared with control hamsters, indicating a cold-induced elevation of thermogenesis. Body mass and fat content were decreased in cold-exposed animals, and serum leptin levels were increased in hamsters exposed to temperatures of -8°C and below in inverse proportion to body fat content. Serum leptin levels were positively correlated with GEI and BAT COX activity in cold-exposed hamsters, but no such relationships were observed in control animals. These findings suggest that cold-exposed hamsters increase food consumption to meet the energy requirements for increased BAT thermogenesis. The increases in serum leptin levels are likely involved in increased thermogenesis in hamsters under cold stress. Cold-exposed hamsters may become leptin resistant, which is associated with impaired regulation of food intake. This new natural model of leptin resistance may also provide insight into the dynamic long-term control of energy homeostasis for animals that do not exhibit seasonal decline in M(b).

Seasonal changes in body mass, energy intake and thermogenesis in Maximowiczi’s voles (Microtus maximowiczii) from the Inner Mongolian grassland

Small mammals inhabiting temperate and arctic regions exhibit annual adaptive adjustments in physiology, anatomy, and behavior. No data on the physiology of Maximowicz's voles (Microtus maximowiczii) are available at present. Here we examined the seasonal changes in body mass, food intake, thermogenic capacity, serum leptin and thyroid hormone levels in wild-captured individuals from Inner Mongolian grassland, China. We further examined the effects of photoperiod on these parameters. Energy intake, resting metabolic rate, nonshivering thermogenesis (NST), and serum tri-iodothyronine (T3) levels increased while serum leptin and body mass decreased in the cold seasons. Serum T3 levels were positively correlated with NST and uncoupling protein 1 (UCP1) contents in brown adipose tissue, and leptin levels were negatively correlated with energy intake and resting metabolic rate. Furthermore, laboratory data showed these changes could be induced by short photoperiod alone. Taken together, our results indicate that Maximowicz's voles can increase thermogenic capacity and energy intake to cope with cold stress. Serum leptin seems to be involved in the regulation of energy intake and changes in T3 level may be important for the variations in NST and/or UCP1. Short photoperiod can serve as a seasonal cue for the winter acclimatization of energy balance in free-living Maximowicz's voles.