In individuals living with obesity, adipose tissue aids in reducing (H_loss) and also serves as a heat storage compartment. Moreover, lean body mass, which has a higher H_prod than adipose tissue plays a crucial role in energy production and thermoregulation. The extent of resistance to the cold remains underexplored in this population, and it is important to understand these responses given the global obesity rise and its health implications. This study aimed to quantify how various body anthropometric variations affected thermal responses in individuals living with obesity during acute compensable cold exposure. A liquid-conditioned suit, connected to a temperature-controlled water circulating bath set at 10°C, was used for 90 min to elicit a compensable cold response in these individuals. Validated methods regarding subjective thermal comfort and sensations, skin temperature (T_skin; °C), heat production (H_prod; kJ ⋅min⁻¹), metabolic fuel selection and shivering intensity were recorded to determine the effect of obesity (and muscle and fat mass) on thermogenic and thermal responses. Our study revealed that individuals with obesity, like their lean counterparts, manifest an increased H_prod during cold exposure by 1.7 ± 1.3 kJ ⋅min⁻¹. However, this increase was observed to be lesser in magnitude among individuals living with obesity compared to lean ones. We also explored the source of fuel during cold exposure and found that carbohydrate and lipid oxidation collectively accounted for a significant proportion of H_prod, with lipid oxidation dominating at 61%, and carbohydrates at 21%. Regarding muscle activity, it was observed that a decrease in T_skin incited an increase in shivering. However, similar to the metabolic responses, shivering in this cohort was much less pronounced than in lean individuals. The study opens avenues for further research, addressing the implications of repeated cold exposure and different lengths, temperatures, or modalities on individuals living with obesity.

No description available.

Haemoglobin and its functions in various organisms is well known; it increases the ability to obtain precious oxygen and it is crucial in aerobic performance. However, if high values of haemoglobin are always beneficial, why is there a large natural variation? This study investigated the effects of varying concentrations of haemoglobin on several stages in the lifespan of Red Junglefowl: egg production and hatching, chicken growth, haemoglobin and summit metabolism. Red Junglefowl were tested for fertility in both eggs laid and eggs hatched. The offspring were individually measured for whole blood haemoglobin concentration and tested for growth and summit metabolism. The results show that there is a difference in haemoglobin after two weeks of age and that growth differs at the same time. High Hb animals do not lay smaller nor fewer eggs than low line birds but their offspring are smaller at the same time as there is a difference in haemoglobin levels. There was also a difference in the summit metabolism between the lines, where the high line animals performed better. Importantly the increase in haemoglobin did effect the growth of the animals negatively, and this would imply that higher levels of haemoglobin is not detrimental to growth.

No description available.

No description available.

More than 30% of the population suffers from obesity, which increases the risk of death and secondary health problems. Body fat [white adipose tissue (WAT) and brown adipose tissue (BAT)] are innervated and regulated by the sympathetic nervous system (SNS). WAT stores energy, while BAT generates heat for thermoregulation. Fat also has sensory innervations, but the roles of sensory nerves are still being elucidated. Hence, understanding the neuroanatomy of the SNS innervations of fat and the neural regulation of fat metabolism will be valuable for advancing obesity treatment. Using trans-synaptic tract tracers with unique fluorescent proteins, we defined and compared the SNS innervations of visceral fat [mesenteric WAT (MWAT)] and subcutaneous fat [inguinal WAT (IWAT)] and of IWAT and interscapular BAT (IBAT) in Siberian hamsters. MWAT and IWAT have moderately shared SNS innervations within the hindbrain, but separate SNS innervations in rostral regions. In contrast, IWAT and IBAT have relatively separate SNS circuitries throughout the brain yet some overlap in SNS nuclei known to regulate thermogenesis. We tested for the presence of functional coordination between IWAT and IBAT defined by overlap in IWAT SNS and IBAT SNS innervations. When IBAT function was impaired by SNS denervation, IWAT SNS drive, thermogenic activity, and beige adipocyte recruitment increased in cold exposed hamsters likely through coordination with IWAT SNS pathways. Conversely, we found that only SNS drive to IWAT increased during acute food deprivation suggesting that populations of SNS neurons singly innervating each fat depot may contribute to differential SNS drive to fat. Lastly, we demonstrated that IWAT sensory nerves mediate the functional coordination between IWAT and IBAT and the regulation of SNS drive to fat. The absence of IWAT sensory feedback via sensory denervation differentially decreased SNS drive to IBAT and IWAT itself, but not to MWAT, retroperitoneal WAT, and epididymal WAT in cold exposed hamsters. Collectively, the studies in this dissertation provide neuroanatomical evidence of separate and shared SNS brain sites likely receiving sensory signaling and regulating SNS drive to fat, and direct evidence of the roles of SNS and sensory nerves innervating fat to energetic homeostasis and thermoregulation.

Embora seja bem estabelecido que a exposição a baixas temperaturas resulte em ativação simpática e hiperglicemia, os mecanismos moleculares envolvidos na regulação neural da produção hepática de glicose ainda não são bem conhecidos. Portanto, o objetivo do presente estudo foi investigar o papel da inervação simpática na regulação de genes e enzimas chaves da neoglicogênese hepática, em roedores expostos agudamente ao frio. Para isso, foram utilizados dois modelos experimentais de desnervação simpática: a simpatectomia química em camundongos induzida pelo tratamento com 6-hidroxidopamina (100 mg.kg-1.dia-1; 1º, 2º e 7º dia de vida pós-natal; i.p). e a desnervação local dos nervos hepáticos por fenol (95%) em ratos. A exposição de camundongos ao frio (4ºC), durante 1, 3 e/ou 6h, induziu hiperglicemia, hipotermia, depleção do conteúdo de glicogênio hepático e ativação da neoglicogênese, estimada pela elevada expressão gênica e atividade das enzimas glicose-6-fosfatase e fosfoenolpiruvato carboxiquinase (PEPCK). Em paralelo, verificou-se que a exposição ao frio induziu um drástico aumento na expressão do RNAm do Nr4a1 e do PGC1-?, dois genes-alvos de CREB que participam do complexo de ativação transcricional dos genes que codificam as enzimas neoglicogênicas estudadas. A simpatectomia não afetou a depleção dos estoques de glicogênio hepático induzida pelo frio, mas reduziu o aumento do conteúdo hepático de noradrenalina e AMPc e acentuou a hipotermia, bem como preveniu a hiperglicemia, sendo este efeito associado ao bloqueio da expressão gênica e atividade da glicose-6-fosfatase e da PEPCK e do RNAm do Nr4a1, em todos os tempos estudados. Resultados bastante semelhantes foram observados em ratos submetidos à lesão dos nervos hepáticos com fenol e expostos ao frio durante 24h. Tanto a adrenalectomia como a adrenodemedulação (remoção da medula da adrenal) não alteraram o efeito estimulatório do frio na atividade e expressão gênica das enzimas neoglicogênicas de camundongos. Porém, em ratos expostos ao frio, a adrenodemedulação bloqueou aIII hiperglicemia e reduziu parcialmente a hiperexpressão dos genes da glicose-6-fosfatase e PEPCK. Estes resultados mostram a importância fisiológica da inervação simpática do fígado de roedores na estimulação do programa gênico da neoglicogênese, durante o estresse térmico agudo. / Although it is well established that exposure to low temperatures leads to sympathetic activation and hyperglycemia, the molecular mechanisms related to the neural regulation of hepatic glucose production remain elusive. Therefore, the goal of the present study was to investigate the role of sympathetic innervation in the regulation of genes and key enzymes of hepatic gluconeogenesis in liver of rodents exposed to acute cold. For this, two experimental models of sympathetic denervation were used: the chemical sympathectomy in mice induced by 6-hydroxydopamine treatment (100 mg.kg-1.day-1; 1º, 2º and 7ºdays of neonatal life; i.p.) and local denervation of hepatic nerves by phenol (95%) in rats. Exposure of mice to cold (4° C) for 1, 3 and / or 6 h induced hyperglycemia, hypothermia, depletion of hepatic glycogen content and activation of gluconeogenesis, estimated by high gene expression and activity of the enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase (PEPCK). In parallel, it was found that exposure to cold induced a dramatic increase in Nr4a1 and PGC1-? mRNA expression, two CREB target genes that participate in the transcriptional activation complex of the genes encoding the gluconeogenesis enzymes studied. The sympathectomy did not affect the depletion of cold-induced hepatic glycogen stores but reduced the hepatic content of noradrenaline and cAMP and increased hypothermia, as well as prevented hyperglycemia, and this effect was associated with the blockade of gene expression and enzymatic activity of glucose-6-phosphatase and PEPCK and Nr4a1 mRNA levels, at all time intervals investigated. Similar results were observed in rats submitted to hepatic nerve damage with phenol and exposed to cold for 24h. Either adrenalectomy or adrenodemedullation (surgical removal of the adrenal medulla) did not alter the stimulatory effect of cold on the activity and gene expression of the gluconeogenesis enzymes of mice. However, in cold-exposed rats, adrenodemedullation blocked hyperglycemia and partially reduced overexpression of the glucose-6-phosphatase and PEPCK mRNA.V These results show the physiological role of the hepatic sympathetic innervation in the transcriptional program associated with gluconeogenesis, during acute thermal stress.

No description available.

Embora seja bem estabelecido que a exposição a baixas temperaturas resulte em ativação simpática e hiperglicemia, os mecanismos moleculares envolvidos na regulação neural da produção hepática de glicose ainda não são bem conhecidos. Portanto, o objetivo do presente estudo foi investigar o papel da inervação simpática na regulação de genes e enzimas chaves da neoglicogênese hepática, em roedores expostos agudamente ao frio. Para isso, foram utilizados dois modelos experimentais de desnervação simpática: a simpatectomia química em camundongos induzida pelo tratamento com 6-hidroxidopamina (100 mg.kg-1.dia-1; 1º, 2º e 7º dia de vida pós-natal; i.p). e a desnervação local dos nervos hepáticos por fenol (95%) em ratos. A exposição de camundongos ao frio (4ºC), durante 1, 3 e/ou 6h, induziu hiperglicemia, hipotermia, depleção do conteúdo de glicogênio hepático e ativação da neoglicogênese, estimada pela elevada expressão gênica e atividade das enzimas glicose-6-fosfatase e fosfoenolpiruvato carboxiquinase (PEPCK). Em paralelo, verificou-se que a exposição ao frio induziu um drástico aumento na expressão do RNAm do Nr4a1 e do PGC1-?, dois genes-alvos de CREB que participam do complexo de ativação transcricional dos genes que codificam as enzimas neoglicogênicas estudadas. A simpatectomia não afetou a depleção dos estoques de glicogênio hepático induzida pelo frio, mas reduziu o aumento do conteúdo hepático de noradrenalina e AMPc e acentuou a hipotermia, bem como preveniu a hiperglicemia, sendo este efeito associado ao bloqueio da expressão gênica e atividade da glicose-6-fosfatase e da PEPCK e do RNAm do Nr4a1, em todos os tempos estudados. Resultados bastante semelhantes foram observados em ratos submetidos à lesão dos nervos hepáticos com fenol e expostos ao frio durante 24h. Tanto a adrenalectomia como a adrenodemedulação (remoção da medula da adrenal) não alteraram o efeito estimulatório do frio na atividade e expressão gênica das enzimas neoglicogênicas de camundongos. Porém, em ratos expostos ao frio, a adrenodemedulação bloqueou aIII hiperglicemia e reduziu parcialmente a hiperexpressão dos genes da glicose-6-fosfatase e PEPCK. Estes resultados mostram a importância fisiológica da inervação simpática do fígado de roedores na estimulação do programa gênico da neoglicogênese, durante o estresse térmico agudo. / Although it is well established that exposure to low temperatures leads to sympathetic activation and hyperglycemia, the molecular mechanisms related to the neural regulation of hepatic glucose production remain elusive. Therefore, the goal of the present study was to investigate the role of sympathetic innervation in the regulation of genes and key enzymes of hepatic gluconeogenesis in liver of rodents exposed to acute cold. For this, two experimental models of sympathetic denervation were used: the chemical sympathectomy in mice induced by 6-hydroxydopamine treatment (100 mg.kg-1.day-1; 1º, 2º and 7ºdays of neonatal life; i.p.) and local denervation of hepatic nerves by phenol (95%) in rats. Exposure of mice to cold (4° C) for 1, 3 and / or 6 h induced hyperglycemia, hypothermia, depletion of hepatic glycogen content and activation of gluconeogenesis, estimated by high gene expression and activity of the enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase (PEPCK). In parallel, it was found that exposure to cold induced a dramatic increase in Nr4a1 and PGC1-? mRNA expression, two CREB target genes that participate in the transcriptional activation complex of the genes encoding the gluconeogenesis enzymes studied. The sympathectomy did not affect the depletion of cold-induced hepatic glycogen stores but reduced the hepatic content of noradrenaline and cAMP and increased hypothermia, as well as prevented hyperglycemia, and this effect was associated with the blockade of gene expression and enzymatic activity of glucose-6-phosphatase and PEPCK and Nr4a1 mRNA levels, at all time intervals investigated. Similar results were observed in rats submitted to hepatic nerve damage with phenol and exposed to cold for 24h. Either adrenalectomy or adrenodemedullation (surgical removal of the adrenal medulla) did not alter the stimulatory effect of cold on the activity and gene expression of the gluconeogenesis enzymes of mice. However, in cold-exposed rats, adrenodemedullation blocked hyperglycemia and partially reduced overexpression of the glucose-6-phosphatase and PEPCK mRNA.V These results show the physiological role of the hepatic sympathetic innervation in the transcriptional program associated with gluconeogenesis, during acute thermal stress.

Abstract The purpose of the study was to examine the amount of cold exposure and factors affecting it at the population level in Finland, to determine what type of cold acclimatisation, if any, develops in urban residents in winter, and to find out whether cold acclimatisation or acclimation has a functional significance on psychological or physical performance. Tasks of low physical activity requiring attention and concentration (cognition, postural control) were assessed in cold. In a cross-sectional population study Finns aged from 25 to 74 years (n=6,951) were queried of their wintertime outdoor exposure duration and factors affecting it. In experimental studies seasonal cold acclimatisation (thermal responses) and its effect on cognition were assessed in the laboratory, where 15 young urban subjects were exposed to cold in winter and summer in bright or dim light. A controlled cold acclimation trial (n=10) was performed to study the effects of repeated exposures to cold on cognitive performance and postural control in young urban subjects. In the Finnish population the average amount of cold exposure in winter represents 4% of the total time. Most of the cold exposure occurs during leisure time and in outdoor occupations (agriculture, forestry, mining, industry, construction). Factors explaining increased occupational cold exposure were: occupation, age and a lesser amount of education. Factors associated with more leisure-time cold exposure were: being employed in outdoor occupations, being a pensioner, housewife, unemployed, practising physical exercise, and reporting at least average health. The experimental studies showed seasonal differences and aggravated thermal responses in urban residents in winter, but did not detect habituation responses typical of cold acclimatisation. In both seasons, acute moderate cold exposure resulted in positive, negative or mixed effects on cognition, reflected as changes in response times and accuracy. Simple cognitive tasks were impaired in cold, and in complex tasks both negative, positive and mixed effects were observed. It is suggested that cold exposure affects cognition through different mechanisms related to either distraction or arousal. Cold exposure increased postural sway by 70-90%, suggesting impaired postural control. Repeated exposures to moderate cold, reducing stress and discomfort and dampening physiological responses, did not markedly affect cognitive performance or postural control.