Metabolic and Hematological Responses to Endotoxin-Induced Inflammation in Chicks Experiencing Embryonic 2,3,7,8-Tetrachlorodibenzodioxin Exposure.

Dioxin exposure during bird embryonic development disrupts immunity as well as mechanisms involved in energy metabolism, potentially affecting negatively acute-phase responses to pathogens. Thus, we hypothesized that embryonic exposure to 2,3,7,8-tetrachlorodibenzodioxin (TCDD) changes the metabolism and blood physiology of domestic chicks, affecting their physiological competence for responding to immune challenges. To test this hypothesis, we injected doses of 0, 1.5, and 3 ng TCDD/egg (based on survival experiments) on embryonic day 4 and then measured O2 consumption and CO2 production for metabolic rate, ventilation, and body temperature (TB ) in 5-d-old chicks. Then, chicks were injected with lipopolysaccharide (LPS, endotoxin) or saline prior to repeating the physiological measurements. A second chick group exposed to identical TCDD and LPS treatments had blood partial pressure of oxygen, partial pressure of carbon dioxide, pH, bicarbonate concentration, lactate concentration, osmolality, hemoglobin concentration, red blood cell concentration, and hematocrit, as well as TB , analyzed at 1 and 5 h after LPS injection. Metabolism in chicks embryonically exposed to 1.5 and 3 ng TCDD/egg was up to 37% higher, whereas body mass of chicks exposed to 3 ng TCDD/egg was approximately 6% lower. Chicks embryonically exposed to 3 ng TCDD/egg challenged with LPS showed a relative persistent hypometabolism accompanied by elimination of the normal hematological and osmotic responses to LPS. We conclude that embryonic exposure to TCDD affects posthatching metabolism as well as impairs metabolic, hematological, and osmotic responses to LPS. Environ Toxicol Chem 2020;39:2208-2220. © 2020 SETAC.

Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure.

Biomarkers are frequently used in ecotoxicology as they allow to study toxicant effects happening at low concentrations of exposure. However, most sublethal studies only evaluate cellular biomarkers which lack evident ecological relevance. We used a multibiomarker approach to estimate the toxic effects of ethoprophos, an organophosphate insecticide commonly used in banana plantations, on the tropical fish Astyanax aeneus (Characidae). We measured biomarkers at sub-individual (cellular) and individual (metabolism, behavior) levels and examined relationships among these responses. A sublethal exposure to ethoprophos caused a significant (54%) reduction of brain Cholinesterase (ChE) activity, reflecting the pesticide's high neurotoxicity. However, other biomarkers like oxidative stress, biotransformation reactions, and resting metabolic rate were not affected. Exposure to ethoprophos modified antipredator behaviors such as escape response and detection avoidance (light/dark preference): exposed fish escaped slower from a simulated attack and preferred brighter areas in a novel tank. The relationship between ChE activity and reaction time suggests that pesticide-induced ChE inhibition reduces escape ability in fish. Our results provide evidence that impacts of organophosphate pesticides on fish ecological fitness can occur even with short exposures at very low concentrations.

Crotamine induces browning of adipose tissue and increases energy expenditure in mice.

Crotamine, originally isolated from rattlesnake venom, has been extensively studied due to its pleiotropic biological properties, and special attention has been paid to its antitumor activity. However, long-term treatment with crotamine was accompanied by a reduction in animal body weight gain and by increases in glucose tolerance. As cancer is commonly associated with cachexia, to preclude the possible cancer cachexia-like effect of crotamine, herein this polypeptide was administered in healthy wild-type C57/BL6 mice by the oral route daily, for 21 days. Reduced body weight gain, in addition to decreased white adipose tissue (WAT) and increased brown adipose tissue (BAT) mass were observed in healthy animals in the absence of tumor. In addition, we observed improved glucose tolerance and increased insulin sensitivity, accompanied by a reduction of plasma lipid levels and decreased levels of biomarkers of liver damage and kidney disfunctions. Importantly, long-term treatment with crotamine increased the basal metabolic rate in vivo, which was consistent with the increased expression of thermogenic markers in BAT and WAT. Interestingly, cultured brown adipocyte cells induced to differentiation in the presence of crotamine also showed increases in some of these markers and in lipid droplets number and size, indicating increased brown adipocyte maturation.

Body composition, resting energy expenditure and inflammatory markers: impact in users of depot medroxyprogesterone acetate after 12 months follow-up

ABSTRACT Objective The aim of this study was to evaluate for 12 months the changes of body weight using Depot Medroxyprogesterone Acetate (DMPA) and if these changes are related to inflammatory markers. Subjects and methods Twenty women of childbearing age who chose the DMPA, without previous use of this method, BMI < 30 kg/m2, and 17 women using IUD TCu 380A, participated in the study. At the baseline and after one year, changes in weight gain, body composition by the bioimpedance electric method, resting energy expenditure (REE) by the indirect calorimetry method, inflammatory markers and HOMA-IR were assessed. Results After 12 months of evaluation, we could observe a significant increase in the DMPA group in weight (3,01 kg) and BMI, while the IUD group’s only significant increase was observed in the BMI. Relative to REE there was an increase of basal metabolic rate (BMR) in both groups after one year. The sub-group DMPA that gained < 3 kg had increased significant weight, BMI and body surface (BS) with respiratory quotient (RQ) reduction, while the sub-group that gained ≥ 3 kg had a significant increase in weight, BMI, BS, fat-free mass, fat mass, BMR, Leptin, HOMA-IR and waist circumference, with RQ significantly reduced. Conclusion Our study found significant changes in weight, body composition and metabolic profile of the population studied in the first 12 months of contraceptive use. These changes mainly increased body weight, leptin levels and HOMA-IR which can contribute to the development of some chronic complications, including obesity, insulin resistance and diabetes mellitus.

Influence of different dialysis modalities in the measurement of resting energy expenditure in patients with acute kidney injury in ICU.

BACKGROUND: Currently, the execution of indirect calorimetry, which is considered the gold standard for measuring energy expenditure, is not indicate during dialysis, and it may interfere on nutritional therapy of these patients. This study aimed to evaluate the resting energy expenditure (REE) in patients with severe acute kidney injury treated by different modalities of dialysis and to identify whether dialysis influences on REE. METHODS: This was a prospective cohort study that evaluated patients admitted in intensive care units with diagnosis of acute kidney injury AKIN-3, mechanically ventilated, and submitted to conventional hemodialysis (CHD), extended hemodialysis (EHD) or high volume peritoneal dialysis (HVPD). Indirect calorimetry was performed at pre dialysis time and during the dialysis procedure. Parameters that could change REE were also evaluated. RESULTS: One-hundred patients undergoing 290 dialysis sessions were evaluated, with mean age 60.3 ± 17 years, 69% were male and 74% have died. There was no significant difference between REE of predialysis time and during dialysis time (2156 ± 659 kcal vs. 2100 ± 634 kcal, respectively, p = 0.15). No difference was observed in the REE before and during dialysis of different modalities. There were no differences between parameters pre and during dialysis of each modality. There was only a difference in norepinephrine dose, which was higher in pre dialysis time in HVPD and EHD modalities, compared with CHD modality. Moreover, during dialysis time, EHD modality had significantly higher VAD compared to other dialysis modalities. CONCLUSION: The three evaluated modalities did not change REE. Indirect calorimetry can be performed during dialysis procedures and there was no difference between ventilation parameters, sedatives use, body temperature and VAD in both moments.

Body composition, resting energy expenditure and inflammatory markers: impact in users of depot medroxyprogesterone acetate after 12 months follow-up.

OBJECTIVE: The aim of this study was to evaluate for 12 months the changes of body weight using Depot Medroxyprogesterone Acetate (DMPA) and if these changes are related to inflammatory markers. SUBJECTS AND METHODS: Twenty women of childbearing age who chose the DMPA, without previous use of this method, BMI < 30 kg/m2, and 17 women using IUD TCu 380A, participated in the study. At the baseline and after one year, changes in weight gain, body composition by the bioimpedance electric method, resting energy expenditure (REE) by the indirect calorimetry method, inflammatory markers and HOMA-IR were assessed. RESULTS: After 12 months of evaluation, we could observe a significant increase in the DMPA group in weight (3,01 kg) and BMI, while the IUD group's only significant increase was observed in the BMI. Relative to REE there was an increase of basal metabolic rate (BMR) in both groups after one year. The sub-group DMPA that gained < 3 kg had increased significant weight, BMI and body surface (BS) with respiratory quotient (RQ) reduction, while the sub-group that gained ≥ 3 kg had a significant increase in weight, BMI, BS, fat-free mass, fat mass, BMR, Leptin, HOMA-IR and waist circumference, with RQ significantly reduced. CONCLUSION: Our study found significant changes in weight, body composition and metabolic profile of the population studied in the first 12 months of contraceptive use. These changes mainly increased body weight, leptin levels and HOMA-IR which can contribute to the development of some chronic complications, including obesity, insulin resistance and diabetes mellitus.

Dietary effect on immunological energetics in mice.

Defense against natural aggressors, such as bacterial infections, requires both energy and an immune-cellular response. However, the question as to how these two components are interconnected in small endotherms by means of the host diet remains only poorly understood. Here, we tested in laboratory mice whether dietary proteins and carbohydrates can modulate the interplay between energy expenditure, food intake and the innate and adaptive immune response when confronting a bacterial challenge (Bacillus Calmette-Guérin, BCG). We observed that mice fed with a high protein diet (HP) developed a better immune response associated to increased numbers of circulating monocytes. In addition, HP diet directly influenced the peripheral blood proportions of both T and B lymphocytes even before the BCG challenge. Interestingly, animals that developed this type of immune response after BCG challenge showed an increased rate of metabolism and food consumption before being challenged. Thus, HP diet induced in non-challenged animals a similar energy expenditure and food intake described by BCG-treated mice. These data suggest that a high amount of proteins in diet can modify the energetic and nutrient dynamic in the host causing a better immune reaction against a microbial challenge.

Cardiorespiratory responses to graded hypoxia in the neotropical fish matrinxã (Brycon amazonicus) and traíra (Hoplias malabaricus) after waterborne or trophic exposure to inorganic mercury.

The growing Hg input in aquatic environments results in high accumulation of mercury in fish tissue and their consumers, which poses a serious risk to humans and ecosystems. The aim of this study was to evaluate the effects of the inorganic mercury exposure on cardiorespiratory responses in two species of neotropical fish ecologically distinct, matrinxã (Brycon amazonicus) and traíra (Hoplias malabaricus). Matrinxãs were exposed to a nominal and sublethal concentration of 0.15 mgL(-1) of HgCl2 for 96 h. Traíras were exposed to trophic doses (each 4 days, during 30 days) of inorganic Hg (0.45 mg as total Hg) using juvenile B. amazonicus as prey vehicle. The metabolic rate (VO2), critical oxygen tensions (PcO2), gill ventilation (VG), tidal volume (VT), respiratory frequency (fR), O2 extraction from the ventilatory current (EO2), and heart rate (fH) were measured under normoxia (140 mm Hg) and graded hypoxia (120, 100, 80, 60, 40, 20, and 10 mm Hg). Regarding matrinxã specifically, the critical point highlighted was tachypnea. In traíras, bradypnea, decreased metabolic rate and O2 extraction, severe bradycardia, and elevated tidal volume were observed in normoxia. Both acute and sub-chronic exposures increased the critical tension of O2 values in more than 100%. In addition, Hg exposures modulated hypoxia-induced responses resulting in impairment of cardio-respiratory system of both species. Thus, mercury, via food or water, decreases the plasticity of the cardiorespiratory responses reducing the survival chances of B. amazonicus and H. malabaricus under hypoxic conditions frequently observed in theirs wild habitats.

High gender -specific susceptibility to curare- a neuromuscular blocking agent.

Curare, a selective skeletal muscle relaxant, has been used clinically to reduce shivering and as an anesthetic auxiliary in abdominal surgery. It is also widely used in animal experiments to block neuromuscular junction activity. Effective doses of curare diminish muscle contraction without affecting brain function, but at higher doses it is known to be lethal. However, the exact dose of curare initiating muscle relaxation vs. lethal effect has not been fully characterized in mice. In this study we carefully examined the dose-response for achieving muscle inactivity over lethality in both male and female mice (C57BL6/J). The most striking finding of this study is that female mice were highly susceptible to curare; both the ED50 and LD50 were at least 3-fold lower than male littermates. This study shows that gender-specific differences can be an important factor when administering skeletal muscle relaxants, particularly curare or other analogous agents targeted to the neuromuscular junction.

High gender -specific susceptibility to curare- a neuromuscular blocking agent

Curare, a selective skeletal muscle relaxant, has been used clinically to reduce shivering and as an anesthetic auxiliary in abdominal surgery. It is also widely used in animal experiments to block neuromuscular junction activity. Effective doses of curare diminish muscle contraction without affecting brain function, but at higher doses it is known to be lethal. However, the exact dose of curare initiating muscle relaxation vs. lethal effect has not been fully characterized in mice. In this study we carefully examined the dose-response for achieving muscle inactivity over lethality in both male and female mice (C57BL6/J). The most striking finding of this study is that female mice were highly susceptible to curare; both the EDm and LDm were at least 3-fold lower than male littermates. This study shows that gender-specific differences can be an important factor when administering skeletal muscle relaxants, particularly curare or other analogous agents targeted to the neuromuscular junction.

Auditory cortex basal activity modulates cochlear responses in chinchillas.

BACKGROUND: The auditory efferent system has unique neuroanatomical pathways that connect the cerebral cortex with sensory receptor cells. Pyramidal neurons located in layers V and VI of the primary auditory cortex constitute descending projections to the thalamus, inferior colliculus, and even directly to the superior olivary complex and to the cochlear nucleus. Efferent pathways are connected to the cochlear receptor by the olivocochlear system, which innervates outer hair cells and auditory nerve fibers. The functional role of the cortico-olivocochlear efferent system remains debated. We hypothesized that auditory cortex basal activity modulates cochlear and auditory-nerve afferent responses through the efferent system. METHODOLOGY/PRINCIPAL FINDINGS: Cochlear microphonics (CM), auditory-nerve compound action potentials (CAP) and auditory cortex evoked potentials (ACEP) were recorded in twenty anesthetized chinchillas, before, during and after auditory cortex deactivation by two methods: lidocaine microinjections or cortical cooling with cryoloops. Auditory cortex deactivation induced a transient reduction in ACEP amplitudes in fifteen animals (deactivation experiments) and a permanent reduction in five chinchillas (lesion experiments). We found significant changes in the amplitude of CM in both types of experiments, being the most common effect a CM decrease found in fifteen animals. Concomitantly to CM amplitude changes, we found CAP increases in seven chinchillas and CAP reductions in thirteen animals. Although ACEP amplitudes were completely recovered after ninety minutes in deactivation experiments, only partial recovery was observed in the magnitudes of cochlear responses. CONCLUSIONS/SIGNIFICANCE: These results show that blocking ongoing auditory cortex activity modulates CM and CAP responses, demonstrating that cortico-olivocochlear circuits regulate auditory nerve and cochlear responses through a basal efferent tone. The diversity of the obtained effects suggests that there are at least two functional pathways from the auditory cortex to the cochlea.

Effects of GABAB receptor agonists and antagonists on glycemia regulation in mice.

γ-Aminobutyric acid (GABA) inhibits insulin secretion through GABA(B) receptors in pancreatic ß-cells. We investigated whether GABA(B) receptors participated in the regulation of glucose homeostasis in vivo. BALB/c mice acutely pre-injected with the GABA(B) receptor agonist baclofen (7.5mg/kg, i.p.) presented glucose intolerance and diminished insulin secretion during a glucose tolerance test (GTT, 2g/kg body weight, i.p.). The GABA(B) receptor antagonist 2-hydroxysaclofen (15 mg/kg, i.p.) improved the GTT and reversed the baclofen effect. Also a slight increase in insulin secretion was observed with 2-hydroxysaclofen. In incubated islets 1.10(-5)M baclofen inhibited 20mM glucose-induced insulin secretion and this effect was reversed by coincubation with 1.10(-5)M 2-hydroxysaclofen. In chronically-treated animals (18 days) both the receptor agonist (5mg/kg/day i.p.) and the receptor antagonist (10mg/kg/day i.p.) induced impaired GTTs; the receptor antagonist, but not the agonist, also induced a decrease in insulin secretion. No alterations in insulin tolerance tests, body weight and food intake were observed with the treatments. In addition glucagon, insulin-like growth factor I, prolactin, corticosterone and growth hormone, other hormones involved in glucose metabolism regulation, were not affected by chronic baclofen or 2-hydroxysaclofen. In islets obtained from chronically injected animals with baclofen, 2-hydroxysaclofen or saline (as above), GABA(B2) mRNA expression was not altered. Results demonstrate that GABA(B) receptors are involved in the regulation of glucose homeostasis in vivo. Treatment with receptor agonists or antagonists, given acutely or chronically, altered glucose homeostasis and insulin secretion alerting to the need to evaluate glucose metabolism during the clinical use of these drugs.

Weight loss and resting energy expenditure in patients with chronic hepatitis C before and during standard treatment.

OBJECTIVE: Infection with hepatitis C virus (HCV) is a serious public health problem worldwide. In clinical studies, weight loss has been reported in 11% to 29% of patients treated with pegylated interferon-α-2a/2b. Few reports have tried to explain such a weight loss. The aim of this study was to evaluate nutritional status, body composition, and resting energy expenditure (REE) in patients with chronic hepatitis C before and during treatment with pegylated interferon and ribavirin. METHODS: This was a prospective study with the evaluation of patients with hepatitis C virus before and after 12 wk of treatment with pegylated interferon and ribavirin. The evaluation consisted of anthropometry (weight, height, body mass index, and waist circumference), and body composition was determined by bioelectrical impedance analysis. The REE of each individual was obtained by indirect calorimetry. To compare the two phases of treatment, the Wilcoxon test was used. The significance level was 5%. RESULTS: Subjects had significant weight loss during treatment with a consequent decrease in body mass index. This weight decrease was accompanied by a significant decrease in body fat and no decrease in fat-free mass. There was a significant decrease in energy intake as assessed by 24-h recall. However, there was no change in REE and in REE corrected for fat-free mass. CONCLUSION: Our study of patients with hepatitis C treatment showed that these patients had significant weight loss and this was not associated with changes in energy expenditure. However, we observed a significant decrease in energy intake, pointing to a possible need for intervention measures to decrease the damage.

Chronic fluoxetine treatment alters cardiovascular functions in unanesthetized rats.

In the present study, we investigated the effects induced by fluoxetine treatment (10 mg/kg) for either 1 or 21 consecutive days on arterial pressure and heart rate basal levels, baroreflex activity, hemodynamic responses to vasoactive agents and cardiovascular responses to acute restraint stress. Mild hypertension was observed after 21 days of treatment, but not after administration for 1 day. Moreover, chronic treatment affected the baroreflex control of heart rate, which was characterized by a reduced reflex tachycardia and an enhanced bradycardiac baroreflex response. The pressor responses to systemic administration of the selective α(1)-adrenoceptor agonist phenylephrine, as well as the depressor responses to systemic infusion of the nitric oxide donor sodium nitroprusside, were reduced after chronic fluoxetine treatment. Fluoxetine treatment for 21 days reduced both the pressor and tachycardiac responses evoked by acute restraint stress. In conclusion, the results indicate the development of mild hypertension after chronic fluoxetine treatment. This effect was followed by changes in the baroreflex control of heart rate and altered vascular responsiveness to pressor and depressor agents, which may explain, at least in part, the increase in arterial pressure. Chronic fluoxetine treatment also affected cardiovascular responses to restraint stress, thus indicating that fluoxetine may affect cardiovascular adaptation under conditions of stress.

[The supplementation of L-carnitine does not promote alterations in the resting metabolic rate and in the use of energetic substrates in physically active individuals]. / A suplementação de L-carnitina não promove alterações na taxa metabólica de repouso e na utilização dos substratos energéticos em indivíduos ativos.

PURPOSE: To investigate the effects of L-carnitine supplementation, over thirty days, on the resting metabolic rate (RMR) and oxidation of free fatty acids (FFA) under rested or exercised conditions. SUBJECTS AND METHODS: Twenty-one overweight active volunteers (40 to 58 years old) were randomized into two groups: supplemented (GS; N = 11; 1,8 g/day of L-carnitine) or placebo (GP; N = 10; maltodextrin). Caloric intake, anthropometry, RMR, VO(2max), respiratory exchange ratio and plasma FFA were measured. RESULTS: No significant changes were found in the caloric intake (-244,66 vs. -126,00 kcal/day), body composition (-0.07 vs. -0.17 kg/m(2)), RMR (0.06 vs. -0.02 kcal/day), respiratory exchange ratio at rest (3.69 vs. -1.01) and exercise (0.01 vs. -0.01) or VO(2max) (0.50 vs. 1.25 mL/kg/min) between GS and GP. Plasma FFA levels were increased under resting conditions only in the GP group (0.27), but no significant changes were observed before or after physical activity in any of the groups. CONCLUSION: Supplementation with L-carnitine caused no changes in the variables analyzed in this study.

A suplementação de L-carnitina não promove alterações na taxa metabólica de repouso e na utilização dos substratos energéticos em indivíduos ativos / The supplementation of L-carnitine does not promote alterations in the resting metabolic rate and in the use of energetic substrates in physically active individuals

OBJETIVO: Avaliar o efeito da suplementação de L-carnitina, por 30 dias, sobre a taxa metabólica de repouso (TMR) e oxidação de ácidos graxos livres (AGL), em repouso e exercício. SUJEITOS E MÉTODOS: Vinte e um voluntários ativos (40 a 58 anos) com sobrepeso foram randomizados em dois grupos: suplementado (GS; N = 11; 1,8 g/dia de L-carnitina) e placebo (GP; N = 10; maltodextrina). Foi feita avaliação da ingestão calórica, antropometria, determinação da TMR, VO2máx, quociente respiratório e AGL plasmáticos. RESULTADOS: Não houve diferença significativa na ingestão (-244,66 vs. -126,00 kcal/dia), composição corporal (-0,07 vs. -0,17 kg/m²), TMR (0,06 vs. -0,02 kcal/ dia), quociente respiratório em repouso (3,69 vs. -1,01) e exercício (0,01 vs. -0,01) e VO2máx (0,50 vs. 1,25 mL/kg/min) para o grupo GS em relação ao GP. Houve aumento dos AGL em repouso no GP (0,27), porém sem diferenças no exercício para os grupos. CONCLUSÃO: Não houve efeito da L-carnitina em nenhuma das variáveis analisadas no estudo.

PURPOSE: To investigate the effects of L-carnitine supplementation, over thirty days, on the resting metabolic rate (RMR) and oxidation of free fatty acids (FFA) under rested or exercised conditions. SUBJECTS AND METHODS: Twenty-one overweight active volunteers (40 to 58 years old) were randomized into two groups: supplemented (GS; N = 11; 1,8 g/day of L-carnitine) or placebo (GP; N = 10; maltodextrin). Caloric intake, anthropometry, RMR, VO2max, respiratory exchange ratio and plasma FFA were measured. RESULTS: No significant changes were found in the caloric intake (-244,66 vs. -126,00 kcal/day), body composition (-0.07 vs. -0.17 kg/m²), RMR (0.06 vs. -0.02 kcal/day), respiratory exchange ratio at rest (3.69 vs. -1.01) and exercise (0.01 vs. -0.01) or VO2max (0.50 vs. 1.25 mL/kg/min) between GS and GP. Plasma FFA levels were increased under resting conditions only in the GP group (0.27), but no significant changes were observed before or after physical activity in any of the groups. CONCLUSION: Supplementation with L-carnitine caused no changes in the variables analyzed in this study.

A TRbeta-selective agonist confers resistance to diet-induced obesity.

Thyroid hormone receptor beta (TRbeta also listed as THRB on the MGI Database)-selective agonists activate brown adipose tissue (BAT) thermogenesis, while only minimally affecting cardiac activity or lean body mass. Here, we tested the hypothesis that daily administration of the TRbeta agonist GC-24 prevents the metabolic alterations associated with a hypercaloric diet. Rats were placed on a high-fat diet and after a month exhibited increased body weight (BW) and adiposity, fasting hyperglycemia and glucose intolerance, increased plasma levels of triglycerides, cholesterol, nonesterified fatty acids and interleukin-6. While GC-24 administration to these animals did not affect food ingestion or modified the progression of BW gain, it did increase energy expenditure, eliminating the increase in adiposity without causing cardiac hypertrophy. Fasting hyperglycemia remained unchanged, but treatment with GC-24 improved glucose tolerance by increasing insulin sensitivity, and also normalized plasma triglyceride levels. Plasma cholesterol levels were only partially normalized and liver cholesterol content remained high in the GC-24-treated animals. Gene expression in liver, skeletal muscle, and white adipose tissue was only minimally affected by treatment with GC-24, with the main target being BAT. In conclusion, during high-fat feeding treatment with the TRbeta-selective agonist, GC-24 only partially improves metabolic control probably as a result of accelerating the resting metabolic rate.

Toxin jararhagin in low doses induces interstitial edema and increases the metabolic rate and red blood cells in mice.

Jararhagin is a metalloproteinase from Bothrops jararaca responsible for hemorrhage, inflammation, necrosis and edema. Effects of low doses of the toxin were analyzed on the energy metabolism of mice as well as its physiological implications. Measures of O(2) consumption (VO(2)) were quantified after 4 and 24h of the jararhagin administration during four weeks. Hematocrit and histology of the lungs were also analyzed after the end of the treatment. Results showed that animals that received subcutaneous doses of jararhagin had significant increase in VO(2) from second (120 ng) and third weeks (60 ng) after 4 and 24h, comparing to control, as well as in the number of erythrocytes after four weeks. Histology of the lungs showed interstitial edema within the alveolar septum. Results suggest that the jararhagin toxin caused an increase in VO(2) and edema of intra-alveolar septum. The increase of the erythrocytes could be a physiological response to adjust the higher necessity of oxygen, due to diffusional abnormalities caused by the edema. Thus, low doses of jararhagin promote endothelial edema which lead to changes in several physiological conditions.

Interplay between metabolic rate and diet quality in the South American fox, Pseudalopex culpaeus.

We studied the metabolic costs associated with the ingestion of peppertree fruits (Schinus molle) in the culpeo fox, Pseudalopex culpaeus, the second largest canid in South America. Throughout its range of distribution, this fox feeds on rodents and other small vertebrates, and also on peppertree fruits, which represent 98% of total fruits consumed in semiarid Chile. Peppertree contains a high diversity of phytochemicals. Foxes feeding on diets containing rats and peppertree fruits (mixed diets) exhibited a 98.9% increase in basal rate of metabolism when compared to rat-acclimated foxes. Thus, acute ingestion of chemically defended fruits has an energetic cost for the fox, reflected in higher values of basal metabolism. Increased metabolic rates may be associated with increased protein synthesis for detoxification and for tissue repair, including the production of biotransformation enzymes.

Obesidad y ácidos grasos en la etiología de la resistencia insulínica / Obesity and fatty acids in the etiology of insulin resistance

Fatty acids, obesity and insulin resistance relationship are discussed. In the last decades fatty acids (FA) have been implicated in the etiology of insulin resistance. Initially, this process was related to FA inhibitory effects on glucose uptake mediated by the FA oxidation metabolites. This mechanism known as the Randle cycle has been presently discarded based on recent evidence for FA effects on glucose metabolism. Now is known that cytosolic lipid content and FA molecular structure determines higher or lower storage and oxidation capacity. Another factor is given by Tumor Necrosis Factor-a, which is overexpressed in animal and human obesity, producing insulin signaling and glucose uptake inhibition. This paper discuss the role played by FA and obesity on insulin resistance, mainly in relation to FA effects on glucose metabolism in the liver, muscle and adipose tissues. In the obesity condition adipose tissue releases higher levels of free FA which in turn stimulates hepatic glucose production. Adipose tissue also, increase TNF-a secretion impairing glucose utilization and insulin signaling. In muscle, cytosolic lipid content activate a Protein Kinase that inhibits the insulin signaling and reduce GLUT-4 translocation. The study of cellular and metabolic changes associated to weight gain and its relationship with insulin resistance etiology are encouraged