Body Fat Stores Research Articles

Insights into pubertal delay in children with Crohn's disease

Delay in onset and progression of puberty is well documented in children with Crohn's disease. This, in turn, has the potential for adversely impacting linear growth and impairing bone accrual, and can have significant effects on the quality of life in these children. Possible reasons for this delay have included undernutrition with poor body fat stores and an ill-defined effect of the inflammatory cytokines involved in the disease process. Animal studies suggest that cytokines and other mediators of inflammation have a suppressant effect on sex hormones, which can be reversed with use of antibody against tumor necrosis factor α (TNF-α). There are little prior data in this regard in children with Crohn's disease.In this issue of The Journal, DeBoer et al provide much needed insight into the problem of pubertal delay associated with Crohn's disease. Children with active disease have low levels of testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone. The sex hormone and gonadotropin levels were negatively associated with the pediatric Crohn's disease activity index, cytokine levels, and measures of inflammation. Following induction of therapy with TNF-α there was a rapid and sustained rise in sex hormone and gonadotropin levels together with improvement in disease activity, and these changes were independent of body mass index or fat mass. Although the results of this study indicate the effects of inflammation on the suppression of sex hormones occurs at the level of gonadotropin regulation, the precise mechanisms involved remain to be identified.The implications of these findings extend beyond Crohn's disease because other chronic inflammatory diseases also can impact pubertal development. Understanding the reasons behind this delay is essential for treatment, which will ultimately significantly improve the lives of affected children.Article page 146▶ Delay in onset and progression of puberty is well documented in children with Crohn's disease. This, in turn, has the potential for adversely impacting linear growth and impairing bone accrual, and can have significant effects on the quality of life in these children. Possible reasons for this delay have included undernutrition with poor body fat stores and an ill-defined effect of the inflammatory cytokines involved in the disease process. Animal studies suggest that cytokines and other mediators of inflammation have a suppressant effect on sex hormones, which can be reversed with use of antibody against tumor necrosis factor α (TNF-α). There are little prior data in this regard in children with Crohn's disease. In this issue of The Journal, DeBoer et al provide much needed insight into the problem of pubertal delay associated with Crohn's disease. Children with active disease have low levels of testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone. The sex hormone and gonadotropin levels were negatively associated with the pediatric Crohn's disease activity index, cytokine levels, and measures of inflammation. Following induction of therapy with TNF-α there was a rapid and sustained rise in sex hormone and gonadotropin levels together with improvement in disease activity, and these changes were independent of body mass index or fat mass. Although the results of this study indicate the effects of inflammation on the suppression of sex hormones occurs at the level of gonadotropin regulation, the precise mechanisms involved remain to be identified. The implications of these findings extend beyond Crohn's disease because other chronic inflammatory diseases also can impact pubertal development. Understanding the reasons behind this delay is essential for treatment, which will ultimately significantly improve the lives of affected children. Article page 146▶ Increases in Sex Hormones during Anti-Tumor Necrosis Factor α Therapy in Adolescents with Crohn's DiseaseThe Journal of PediatricsVol. 171PreviewTo evaluate children with Crohn's disease for inverse relationships between systemic inflammatory cytokines and sex hormone regulation in the context of anti-tumor necrosis factor α (TNF-α) therapy. Full-Text PDF

Role of the BAHD1 Chromatin-Repressive Complex in Placental Development and Regulation of Steroid Metabolism.

BAHD1 is a vertebrate protein that promotes heterochromatin formation and gene repression in association with several epigenetic regulators. However, its physiological roles remain unknown. Here, we demonstrate that ablation of the Bahd1 gene results in hypocholesterolemia, hypoglycemia and decreased body fat in mice. It also causes placental growth restriction with a drop of trophoblast glycogen cells, a reduction of fetal weight and a high neonatal mortality rate. By intersecting transcriptome data from murine Bahd1 knockout (KO) placentas at stages E16.5 and E18.5 of gestation, Bahd1-KO embryonic fibroblasts, and human cells stably expressing BAHD1, we also show that changes in BAHD1 levels alter expression of steroid/lipid metabolism genes. Biochemical analysis of the BAHD1-associated multiprotein complex identifies MIER proteins as novel partners of BAHD1 and suggests that BAHD1-MIER interaction forms a hub for histone deacetylases and methyltransferases, chromatin readers and transcription factors. We further show that overexpression of BAHD1 leads to an increase of MIER1 enrichment on the inactive X chromosome (Xi). In addition, BAHD1 and MIER1/3 repress expression of the steroid hormone receptor genes ESR1 and PGR, both playing important roles in placental development and energy metabolism. Moreover, modulation of BAHD1 expression in HEK293 cells triggers epigenetic changes at the ESR1 locus. Together, these results identify BAHD1 as a core component of a chromatin-repressive complex regulating placental morphogenesis and body fat storage and suggest that its dysfunction may contribute to several human diseases.

Leptin regulates energy intake but fails to facilitate hibernation in fattening Daurian ground squirrels (Spermophilus dauricus)

Body fat storage before hibernation affects the timing of immergence in Daurian ground squirrels (Spermophilus dauricus). Leptin is an adipose signal and plays vital role in energy homeostasis mainly by action in brain. To test the hypothesis that leptin plays a role in facilitating the process of hibernation, squirrels were administrated with recombinant murine leptin (1μg/day) through intracerebroventricular (ICV) injection for 12 days during fattening. From day 7 to 12, animals were moved into a cold room (5±1°C) with constant darkness which functioned as hibernaculum. Energy intake, body mass and core body temperature (Tb) were continuously monitored throughout the course of experiment. Resting metabolic rate (RMR) was measured under both warm and cold conditions. At the end of leptin administration, we measured the serum concentration of hormones related to energy regulation, mRNA expression of hypothalamic neuropeptides and uncoupling protein 1 (UCP1) levels in brown adipose tissue (BAT). Our results showed that during leptin administration, the cumulative food intake and increase of body mass were suppressed while Tb and RMR were unaltered. The proportion of torpid squirrels was not different between two groups. At the end of leptin administration, the expressions of hypothalamic neuropeptide Y and agouti gene-related protein were suppressed. There were no differences in UCP1 mRNA expression or protein content in BAT between groups. Our data suggest that leptin can affect energy intake via hypothalamic neuropeptides, but is not involved in the initiation of hibernation in fattening Daurian ground squirrels.

Bovine lactoferrin suppresses high-fat diet induced obesity and modulates gut microbiota in C57BL/6J mice

Gut microbiota has been suggested to participate in the pathogenesis of low-grade inflammation and obesity; bovine lactoferrin (bLF) as a dietary supplement is well known for its anti-microbial and prebiotic potency. However, the role of bLF in obesity as a prebiotic compound has not been investigated previously. We report that oral administration of 100 mg/kg BW bLF for 12 weeks decreased body weight gain and fat storage, reduced the blood cholesterol and glucose concentrations, and alleviated liver steatosis. The overexpression of leptin and plasminogen activator inhibitor (PAI-I) was suppressed, which could be attributed to decreased lipopolysaccharide (LPS) translocation and gut inflammation by bLF through positive modulation on gut microbiota, i.e. increasing the number of Bifidobacterium spp. and modestly inhibiting the growth of Enterobacteriales. Our results demonstrated that oral administration with bLF positively modulated gut microbiota, reduced inflammation and regulated lipid and glucose metabolism in high-fat diet induced obese mice.

Restriction of rapid eye movement sleep during adolescence increases energy gain and metabolic efficiency in young adult rats.

What is the central question of this study? Sleep curtailment in infancy and adolescence may lead to long-term risk for obesity, but the mechanisms involved have not yet been determined. This study examined the immediate and long-term metabolic effects produced by sleep restriction in young rats. What is the main finding and its importance? Prolonged sleep restriction reduced weight gain (body fat stores) in young animals. After prolonged recovery, sleep-restricted rats tended to save more energy and to store more fat, possibly owing to increased gross food efficiency. This could be the first step to understand this association. Sleep curtailment is associated with obesity and metabolic changes in adults and children. The aim of the present study was to evaluate the immediate and long-term metabolic alterations produced by sleep restriction in pubertal male rats. Male Wistar rats (28 days old) were allocated to a control (CTL) group or a sleep-restricted (SR) group. This was accomplished by the single platform technique for 18 h per day for 21 days. These groups were subdivided into the following four time points for assessment: sleep restriction and 1, 2 and 4 months of recovery. Body weight and food intake were monitored throughout the experiment. At the end of each time period, blood was collected for metabolic profiling, and the carcasses were processed for measurement of body composition and energy balance. During the period of sleep restriction, SR animals consumed less food in the home cages. This group also displayed lower body weight, body fat, triglycerides and glucose levels than CTL rats. At the end of the first month of recovery, despite eating as much as CTL rats, SR animals showed greater energy and body weight gain, increased gross food efficiency and decreased energy expenditure. At the end of the second and fourth months of recovery, the groups were no longer different, except for energy gain and gross food efficiency, which remained higher in SR animals. In conclusion, sleep restriction affected weight gain of young animals, owing to reduction of fat stores. Two months were sufficient to recover this deficit and to reveal that SR rats tended to save more energy and to store more fat.

Individual and contextual correlates of obesity-related behaviours and obesity: the SPOTLIGHT project.

Individual and contextual correlates of obesity-related behaviours and obesity: the SPOTLIGHT project.

Adipogenic function and other biologic effects of insulin

Studies on experimental animals with knockout of the insulin receptor gene Insr (in the whole body or in certain tissues) and/or related genes encoding proteins involved in realization of insulin signal transduction in target cells, have made an important contribution to the elucidation of insulin regulation of metabolism, particularly fat metabolism. Since the whole insulin secreted by b-cells, together with the products of gastrointestinal tract digestion of proteins, fats, and carbohydrates reach the liver, the latter is the first organ on which this hormone acts. The liver employs released amino acids for synthesis of proteins, including apoproteins for various lipoproteins. Glucose is used for synthesis of glycogen, fatty acids, and triglycerides, which enter all the organs in very low density lipoproteins (VLDL). The LIRKO mice with knockout of the Insr gene in the liver demonstrated inhibition of synthesis of macromolecular compounds from amino acids, glucose, and fatty acids. Low molecular weight substances demonstrated increased entry to circulation, and together with other disorders induced hyperglycemia. In LIRKO mice blood glucose levels and glucose tolerance demonstrated time-dependent normalization and at later stages the increase in glucose levels was replaced by hypoglycemia. These changes can be well explained if we take into consideration that one of the main functions of insulin consists in stimulation of energy accumulation by means of activation of triglyceride deposition in adipose tissue. FIRKO mice with selective knockout of adipose tissue Insr were characterized by decreased uptake of glucose in adipocytes, and its transformation into lipids. However, the level of body fat in animals remained normal, possibly due to preserved insulin receptor in the liver and insulin-induced activation of triglyceride production which maintained normal levels of body fat stores, the effective functioning of adipose tissue and secretion of leptin by adipocytes during inhibition of glucose transformation into triglyceride in adipose tissue. Knockout of the Insr gene in muscles blocked glucose uptake by myocytes, but it did not induce hyperglycemia, probably due to the increase in glucose uptake by other organs, which retained the insulin receptor, and induced some increase in fat resources in adipose tissue. Similar results were obtained in mice with knockout the glucose transporter 4 GLUT4 in muscle and/or adipose tissue. Insulin microinjections in the brain, in the cerebral ventricle 4 (ICV) and mediobasal hypothalamus (MBH) did not affect the insulin levels in the general circulation, but effectively activated lipogenesis and inhibited lipolysis in adipose tissue. They induced obesity, similar to conventional obesity when the insulin levels increased. These results may serve as additional evidence for importance of the adipogenic insulin function in mechanisms of regulation of general metabolism.

Adiponectin Secretion in HIV-Infected Subjects with or without Antiretroviral Treatment and Illicit Substance Use: Clinical Review and Update

Adiponectin (Acrp30) is a novel polypeptide classified among adipokines that are chiefly secreted by adipocytes within adipose tissue. Besides the adipose tissue, levels of the adipocytokine also circulate in human plasma. Functionally, Acrp30 possesses a primary role in regulation of body fat stores with its anti-inflammatory, glucose and lipid metabolism and weight loss effects. Thus, circulating Acrp30 levels govern obesity and metabolic abnormalities including; dyslipidaemia, cardiovascular disorders and renal disease. A lipodystrophic syndrome including metabolic derangements are common features presenting in HIV-infected patients on antiretroviral therapy (ART). Decreased Acrp30 levels have been documented in lipodystrophic patients as a consequence of adverse effects attributable to various antiretroviral agents. Interestingly, Acrp30 levels are revealed to be suppressed in HIV-infected patients relative to healthy persons even prior to HAART commencement, indicative of HIV infection itself playing a role in Acrp30 dysregulation. On the contrary, circulating Acrp30 levels inversely correlate with body fat composition in healthy non-obese individuals. Thus, lowered Acrp30 concentrations are associated with weight accumulation in obese subjects. More importantly, illicit drug and substance use has been revealed to accelerate HIV disease progression while also impairing Acrp30 production within the adipose tissue. Consequently, these observations collectively portray Acrp30 as a metabolic correlate of adipose tissue inflammation and low fat store during episodes of HIV infection, lypodystrophyic syndrome and illicit substance use. Therapeutic interventions should identify new approaches to restore Acrp30 production and supply during the aforementioned events.

The adipogenic function and other biological effects of insulin

Studies on experimental animals with knockout of the insulin receptor gene (Insr) in the whole body or in certain tissues and/or related genes encoding proteins involved in realization of insulin signal transduction in target cells, have made an important contribution to the elucidation of insulin regulation of metabolism, particularly fat metabolism. Since the whole insulin secreted by β-cells, together with the products of gastrointestinal tract digestion of proteins, fats, and carbohydrates reaches in the liver, the latter is the first organ on which this hormone acts. The liver employs released amino acids for synthesis of proteins, including apo-proteins for various lipoproteins. Glucose is used for synthesis of glycogen, fatty acids, and triglycerides, which enter all the organs in very low density lipoproteins (VLDL). The LIRKO mice with knockout of the insr gene in the liver demonstrated inhibition of synthesis of macromolecular compounds from amino acids, glucose, and fatty acids. Low molecular weight substances demonstrated increased entry to circulation, and together with other disorders induced hyperglycemia. In LIRKO mice blood glucose levels and glucose tolerance demonstrated time-dependent normalization and at later stages the increase in glucose levels was replaced by hypoglycemia. These changes can be well explained if we take into consideration that one of the main functions of insulin consists in stimulation of energy accumulation by means of activation of triglyceride deposition in adipose tissue. FIRKO mice with selective knockout of adipose tissue Insr were characterized by decreased uptake of glucose in adipocytes, and its transformation into lipids. However, the level of body fat in animals remained normal, possibly due to preserved insulin receptor in the liver and insulin-induced activation of triglyceride production which maintained normal levels of body fat stores, the effective functioning of adipose tissue and secretion of leptin by adipocytes during inhibition of glucose transformation into triglyceride in adipose tissue. Knockout of the Insr gene in muscles blocked glucose uptake by myocytes, but it did not induce hyperglycemia, probably due to the increase in glucose uptake by other organs, which retained the insulin receptor, and induced some increase in fat resources in adipose tissue. Similar results were obtained in mice with knockout the glucose transporter 4 GLUT4 in muscle and/or adipose tissue. Insulin microinjections in the brain, in the cerebral ventricle 4 (CVI) and mediobasal hypothalamus (MBH) did not affect the insulin levels in the general circulation, but effectively activate lipogenesis and inhibited lipolysis in adipose tissue. They induced obesity, similar to conventional obesity when the insulin levels increased. These results may serve as an additional confirmation of the importance of the adipogenic insulin function in mechanisms of regulation of general metabolism.

Physiological leptin resistance

Leptin is an adipose tissue-derived hormone whose circulating levels correlate with the amount of body fat stores. The main function of this adipokine is to regulate energy metabolism. By modulating the expression of orexigenic and anorexigenic neuropeptides in the hypothalamus, leptin reduces appetite. It also increases energy expenditure, contributing to the decrease of body fat and body weight. Mutations in the leptin receptor gene or prolonged consumption of a high-fat diet may impair leptin action, leading to leptin resistance. Resistance to leptin can also be an adaptive response that occurs in seasonal animals and in pregnant mammals. Reversible insensitivity to the satiety signal of leptin promotes hyperphagia, which is essential for animals living in dynamic environments and experiencing seasonal variation in food availability, since it allows them to forage intensely when food is abundant and accumulate fat reserves necessary to survive periods when food is scarce. Moreover, leptin resistance and subsequent hyperphagia develop during pregnancy in order to meet the energy needs of the growing fetus. Physiological leptin resistance may be due to impaired transport of leptin across the blood-brain barrier and/or to decreased sensitivity of the hypothalamus to this hormone resulting from an inhibition of leptin signalling in hypothalamic neurons. In pregnancy, an increased resistance to leptin action is also mediated by the binding of this adipokine to its placenta-derived soluble receptor. Reduced entry of leptin into the brain as well as alterations in the leptin signalling pathway in the hypothalamus leads to a transient decrease in sensitivity to this hormone preventing appetite suppression.

Inverse Relationship of the CMKLR1 Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance.

Background. In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet. Methods. Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2−ΔΔCT method. Results. Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05. Conclusion. The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.

Socio-cultural and Environmental Factors Contribute to Increased Body Weights and Obesity

Obesity may be simply defined as the degree of body fat storage associated with elevated health risks. Obesity was widely seen as a symbol of wealth in some parts of the world. Now, it is a serious health problem throughout the world. It is high time to think about it and make changes in their lifestyle to have a healthy future.

Sexual Size Dimorphism and Body Condition in the Australasian Gannet.

Sexual size dimorphism is widespread throughout seabird taxa and several drivers leading to its evolution have been hypothesised. While the Australasian Gannet (Morus serrator) has previously been considered nominally monomorphic, recent studies have documented sexual segregation in diet and foraging areas, traits often associated with size dimorphism. The present study investigated the sex differences in body mass and structural size of this species at two colonies (Pope’s Eye, PE; Point Danger, PD) in northern Bass Strait, south-eastern Australia. Females were found to be 3.1% and 7.3% heavier (2.74 ± 0.03, n = 92; 2.67 ± 0.03 kg, n = 43) than males (2.66 ± 0.03, n = 92; 2.48 ± 0.03 kg, n = 43) at PE and PD, respectively. Females were also larger in wing ulna length (0.8% both colonies) but smaller in bill depth (PE: 2.2%; PD: 1.7%) than males. Despite this dimorphism, a discriminant function provided only mild accuracy in determining sex. A similar degree of dimorphism was also found within breeding pairs, however assortative mating was not apparent at either colony (R 2 < 0.04). Using hydrogen isotope dilution, a body condition index was developed from morphometrics to estimate total body fat (TBF) stores, where TBF(%) = 24.43+1.94*(body mass/wing ulna length) – 0.58*tarsus length (r 2 = 0.84, n = 15). This index was used to estimate body composition in all sampled individuals. There was no significant difference in TBF(%) between the sexes for any stage of breeding or in any year of the study at either colony suggesting that, despite a greater body mass, females were not in a better condition than males. While the driving mechanism for sexual dimorphism in this species is currently unknown, studies of other Sulids indicate segregation in foraging behaviour, habitat and diet may be a contributing factor.

Protein-energy malnutrition at mid-adulthood does not imprint long-term metabolic consequences in male rats.

The long-term effects of the development of chronic metabolic diseases such as type 2 diabetes and obesity have been associated with nutritional insults in critical life stages. In this study, we evaluated the effect of a low-protein diet on metabolism in mid-adulthood male rats. At 90days of age, Wistar male rats were fed a low-protein diet (4.0%, LP group) for 30days, whereas control rats were fed a normal-protein diet (20.5%, NP group) throughout their lifetimes. To allow for dietary rehabilitation, from 120 to 180days of age, the LP rats were fed a normal-protein diet. Then, we measured body composition, fat stores, glucose-insulin homeostasis and pancreatic islet function. At 120days of age, just after low-protein diet treatment, the LP rats displayed a strong lean phenotype, hypoinsulinemia, as assessed under fasting and glucose tolerance test conditions, as well as weak pancreatic islet insulinotropic response to glucose and acetylcholine (p<0.01). At 180days of age, after poor-protein diet rehabilitation, the LP rats displayed a slight lean phenotype (p<0.05), which was associated with a high body weight gain (p<0.001). Additionally, fat pad accumulation, glycemia and insulinemia, as well as the pancreatic islet insulinotropic response, were not significantly different between the LP and NP rats (p>0.05). Taken together, the present data suggest that the effects of dietary restriction as a stressor in adulthood are reversible with dietary rehabilitation, indicating that adulthood is not a sensitive or critical time window for metabolic programming.

Behavioural and physiological responses of wood mice (Apodemus sylvaticus) to experimental manipulations of predation and starvation risk

Body weight and the levels of stored body fat have fitness consequences. Greater levels of fat may provide protection against catastrophic failures in the food supply, but they may also increase the risk of predation. Animals may therefore regulate their fatness according to their perceived risks of predation and starvation: the starvation–predation trade-off model. We tested the predictions of this model in wood mice (Apodemus sylvaticus) by experimentally manipulating predation risk and starvation risk. We predicted that under increased predation risk individuals would lose weight and under increased starvation risk they would gain it. We simulated increased predation risk by playing the calls made by predatory birds (owls: Tyto alba and Bubo bubo) to the mice. Control groups included exposure to calls of a non-predatory bird (blackbird: Turdus merula) or silence. Mice exposed to owl calls at night lost weight relative to the silence group, mediated via reduced food intake, but exposure to owl calls in the day had no significant effect. Exposure to blackbird calls at night also resulted in weight loss, but blackbird calls in the day had no effect. Mice seemed to have a generalised response to bird calls at night irrespective of their actual source. This could be because in the wild any bird calling at night will be a predation risk, and any bird calling in the day would not be, because at that time the mice would normally be resting, and hence not exposed to avian predators. Consequently, mice have not evolved to distinguish different types of call but only to respond to the time of day that they occur. Mice exposed to stochastic 24h starvation events altered their behaviour (reduced activity) during the refeeding days that followed the deprivation periods to regain the lost mass. However, they only marginally elevated their food intake and consequently had reduced body weight/fat storage compared to that of the control unstarved group. This response may have been constrained by physiological factors (alimentary tract absorption capacity) or behavioural factors (perceived risk of predation). Overall the responses of the mice appeared to provide limited support for the starvation–predation trade-off model, and suggest that wood mice are much more sensitive to predation risk than they are to starvation risk.

Advanced seasonal reproductive development in a male urban bird is reflected in earlier plasma luteinizing hormone rise but not energetic status

Urban animals inhabit an environment considerably different than do their non-urban conspecifics, and to persist urban animals must adjust to these novel environments. The timing of seasonal reproductive development (i.e., growth of gonads and secondary sex organs) is a fundamental determinant of the breeding period and is frequently advanced in urban bird populations. However, the underlying mechanism(s) by which birds adjust the timing of reproductive development to urban areas remain(s) largely unknown. Here, we compared the timing of vernal reproductive development in free-ranging urban and non-urban male Abert’s Towhees, Melozone aberti, in Phoenix, Arizona, USA, and tested the non-mutually exclusive hypotheses that earlier reproductive development is due to improved energetic status and/or earlier increase in endocrine activity of the reproductive system. We found that urban birds initiated testicular development earlier than non-urban birds, but this disparity was not associated with differences in body condition, fat stores, or innate immune performance. These results provide no support for the hypothesis that energetic constraints are responsible for delayed reproductive development of non-urban relative to urban male Abert’s Towhees. Urban birds did, however, increase their plasma luteinizing hormone, but not plasma testosterone, earlier than non-urban birds. These findings suggest that adjustment to urban areas by Abert’s Towhees involves increases in the endocrine activity of the anterior pituitary gland and/or hypothalamus earlier than non-urban towhees.

Vagotomy ameliorates islet morphofunction and body metabolic homeostasis in MSG-obese rats.

The parasympathetic nervous system is important for β-cell secretion and mass regulation. Here, we characterized involvement of the vagus nerve in pancreatic β-cell morphofunctional regulation and body nutrient homeostasis in 90-day-old monosodium glutamate (MSG)-obese rats. Male newborn Wistar rats received MSG (4 g/kg body weight) or saline [control (CTL) group] during the first 5 days of life. At 30 days of age, both groups of rats were submitted to sham-surgery (CTL and MSG groups) or subdiaphragmatic vagotomy (Cvag and Mvag groups). The 90-day-old MSG rats presented obesity, hyperinsulinemia, insulin resistance, and hypertriglyceridemia. Their pancreatic islets hypersecreted insulin in response to glucose but did not increase insulin release upon carbachol (Cch) stimulus, despite a higher intracellular Ca2+ mobilization. Furthermore, while the pancreas weight was 34% lower in MSG rats, no alteration in islet and β-cell mass was observed. However, in the MSG pancreas, increases of 51% and 55% were observed in the total islet and β-cell area/pancreas section, respectively. Also, the β-cell number per β-cell area was 19% higher in MSG rat pancreas than in CTL pancreas. Vagotomy prevented obesity, reducing 25% of body fat stores and ameliorated glucose homeostasis in Mvag rats. Mvag islets demonstrated partially reduced insulin secretion in response to 11.1 mM glucose and presented normalization of Cch-induced Ca2+ mobilization and insulin release. All morphometric parameters were similar among Mvag and CTL rat pancreases. Therefore, the higher insulin release in MSG rats was associated with greater β-cell/islet numbers and not due to hypertrophy. Vagotomy improved whole body nutrient homeostasis and endocrine pancreatic morphofunction in Mvag rats.

Analysis of Sugar Intake and Resting Energy Expenditure in Adult Males During a 5-week Period

High levels of sugar intake have been shown to stimulate energy conservation processes and may progressively enhance body fat storage. PURPOSE: To assess the influence of sugar intake on metabolic processes during a 5-week period. METHODS: Twenty-nine healthy adult males recorded dietary intake and pedometer (PED) data for two week days and one weekend day at baseline (weeks 1 and 2) and again after 5-weeks. The recorded days were randomly selected each week for each participant. The change (5 weeks - baseline) in sugar intake was recorded and the participants were then divided into two groups based on whether sugar intake was increased (IS; n=10; age: 35.6±3.9 years) or decreased (DS; n=19; age: 34.6±7.8 years) during the 5-week period. Body height, mass, percent body fat (BF%), and resting energy expenditure (REE) were measured at baseline and again at 5 weeks. RESULTS: No differences in sugar intake (IS: 59.0±16.4 g; DS: 70.4±29.5 g), PED (IS: 7055.1±2387.0 steps; DS: 7061.1±3881.3 steps), body mass index (BMI) (IS: 27.7±3.8 kg/m2; DS: 26.8±3.8 kg/m2), BF% (IS: 27.8±6.8%; DS: 24.8±9.3%), or REE (IS: 1628.5±272.4 kcal; DS: 1672.9±252.9 kcal) were found between groups at baseline (P>0.05). Sugar intake, however, was significantly different between IS and DS at 5 weeks (P0.05). Conversely, the change in sugar intake was significantly different between IS (25.4±17.7 g) and DS (-16.3±12.8 g) (P<0.05). CONCLUSIONS: REE did not change based on sugar intake during the 5-week period. These data, however, present some interesting evidence that lead to further questions regarding sugar intake and metabolic processes. Future research should include more subjects observed over a longer period of time to expand on these data and to explore the potential progressive influence of sugar intake on health and body composition. Supported by FP7-PEOPLE-2012-IRSES grant no. 319010; FP7-PEOPLE-2013-IRSES grant no. 612547.

Nutritional status in university students: its relation to the number of daily intakes and macronutrients consumption

There is increasing scientific evidence that nutrition influence positive and negative on health along life. Many studies have reported that the student population is a particularly vulnerable group from the nutritional point of view, due to it is characterized by meal skipping frequently and nibble between eating occasions. to establish the relationship between the number of daily dietary intakes and nutritional status in male students aged 23 to 33 years of the National Technological University, in the city of Córdoba, in 2013. in order to achieve this aim, a prospective, cross-sectional and descriptive correlational design was used. Descriptive and inferential analysis were applied by using multiple logistic regression models. Almost 50% of the sample analyzed presented overweight (OW) and 40% high body fat (BF). In relation to the intakes numbers, the students that take less than 4 and more than 6 had 2 times more chance of presenting overweight and high body fat. It was found that as age increases it also does the Body Fat Storage, whereas diminished physical activity increases the chance of having high Body Mass Index and Body Fat. Moreover, high ingestion of carbohydrates increases the chance of high Body Fat and Overweight, and a high intake of protein and lipids increases the risk of high Body Fat. it is recognized that high or low number of daily intakes than recommended, low level of physical activity, high consumption of carbohydrates and having more than 29 years is related to high overweight and body fat.

Diet-induced obesity causes metabolic impairment independent of alterations in gut barrier integrity.

The causal relationship between diet-induced obesity and metabolic disorders is not clear yet. One hypothesis is whether the obese state or high-fat diet per se affects intestinal barrier function provoking metabolic comorbidities. In three independent experiments with AKR/J, SWR/J, or BL/6J mice, we addressed the impact of genetic background, excess body fat storage, duration of high-fat feeding, and quality/quantity of dietary fat on glucose tolerance and gut barrier integrity in vivo and ex vivo. Impaired glucose tolerance in diet-induced obese BL/6J and AKR/J mice was not accompanied by an altered intestinal barrier function. Enforced dietary challenge by prolonged feeding and increasing fat quantity in BL/6J mice still failed to aggravate metabolic and intestinal deterioration. Despite a low-grade inflammatory status in adipose tissue, barrier function of BL/6J mice fed lard high-fat diet revealed no evidence for a diet-induced loss in barrier integrity. None of our results provided any evidence that gut barrier function is a subject to dietary regulation and obesity per se seems not to cause gut barrier impairment.