Water deprivation induces appetite and alters metabolic strategy in Notomys alexis : unique mechanisms for water production in the desert

Like many desert animals, the spinifex hopping mouse, Notomys alexis, can maintain water balance without drinking water. The role of the kidney in producing a small volume of highly concentrated urine has been well-documented, but little is known about the physiological mechanisms underpinning the metabolic production of water to offset obligatory water loss. In Notomys, we found that water deprivation (WD) induced a sustained high food intake that exceeded the pre-deprivation level, which was driven by parallel changes in plasma leptin and ghrelin and the expression of orexigenic and anorectic neuropeptide genes in the hypothalamus; these changed in a direction that would stimulate appetite. As the period of WD was prolonged, body fat disappeared but body mass increased gradually, which was attributed to hepatic glycogen storage. Switching metabolic strategy from lipids to carbohydrates would enhance metabolic water production per oxygen molecule, thus providing a mechanism to minimize respiratory water loss. The changes observed in appetite control and metabolic strategy in Notomys were absent or less prominent in laboratory mice. This study reveals novel mechanisms for appetite regulation and energy metabolism that could be essential for desert rodents to survive in xeric environments.

n-3 LC-PUFA deposition efficiency and appetite regulating hormones are modulated by the dietary lipid source during rainbow trout grow-out and finishing periods

Largely attributable to concerns surrounding sustainability, the utilisation of omega-3 long-chain polyunsaturated fatty acid-rich (n-3 LC-PUFA) fish oils in aquafeeds for farmed fish species is an increasingly concerning issue. Therefore, strategies to maximise the deposition efficiency of these key health beneficial fatty acids are being investigated. The present study examined the effects of four vegetable-based dietary lipid sources (linseed, olive, palm and sunflower oil) on the deposition efficiency of n-3 LC-PUFA and the circulating blood plasma concentrations of the appetite-regulating hormones, leptin and ghrelin, during the grow-out and finishing phases in rainbow trout culture. Minimal detrimental effects were noted in fish performance; however, major modifications were apparent in tissue fatty acid compositions, which generally reflected that of the diet. These modifications diminished somewhat following the fish oil finishing phase, but longer-lasting effects remained evident. The fatty acid composition of the alternative oils was demonstrated to have a modulatory effect on the deposition efficiency of n-3 LC-PUFA and on the key endocrine hormones involved in appetite regulation, growth and feed intake during both the grow-out and finishing phases. In particular, n-6 PUFA (sunflower oil diet) appeared to ‘spare’ the catabolism of n-3 LC-PUFA and, as such, resulted in the highest retention of these fatty acids, ultimately highlighting new nutritional approaches to maximise the maintenance of the qualitative benefits of fish oils when they are used in feeds for aquaculture species.

Uteroplacental insufficiency leads to hypertension, but not glucose intolerance or impaired skeletal muscle mitochondrial biogenesis, in 12-month-old rats

Growth restriction impacts on offspring development and increases their risk of disease in adulthood which is exacerbated with "second hits." The aim of this study was to investigate if blood pressure, glucose tolerance, and skeletal muscle mitochondrial biogenesis were altered in 12-month-old male and female offspring with prenatal or postnatal growth restriction. Bilateral uterine vessel ligation induced uteroplacental insufficiency and growth restriction in offspring (Restricted). A sham surgery was also performed during pregnancy (Control) and some litters from sham mothers had their litter size reduced (Reduced litter), which restricted postnatal growth. Growth-restricted females only developed hypertension at 12 months, which was not observed in males. In Restricted females only homeostasis model assessment for insulin resistance was decreased, indicating enhanced hepatic insulin sensitivity, which was not observed in males. Plasma leptin was increased only in the Reduced males at 12 months compared to Control and Restricted males, which was not observed in females. Compared to Controls, leptin, ghrelin, and adiponectin were unaltered in the Restricted males and females, suggesting that at 12 months of age the reduction in body weight in the Restricted offspring is not a consequence of circulating adipokines. Skeletal muscle PGC-1α levels were unaltered in 12-month-old male and female rats, which indicate improvements in lean muscle mass by 12 months of age. In summary, sex strongly impacts the cardiometabolic effects of growth restriction in 12-month-old rats and it is females who are at particular risk of developing long-term hypertension following growth restriction.

Dietary whey protein lessens several risk factors for metabolic diseases: a review

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Leptina, ghrelina e exercício físico

A obesidade é atualmente um problema de saúde pública que provoca sérias conseqüências sociais, físicas e psicológicas. A etiologia da obesidade não é de fácil identificação, uma vez que a mesma é caracterizada como doença multifatorial de complexa interação entre fatores comportamentais, culturais, genéticos, fisiológicos e psicológicos. Recentes avanços na área de endocrinologia e metabolismo mostram que, diferentemente do que se acreditava há alguns anos, o adipócito sintetiza e libera diversas substâncias, não sendo apenas uma célula armazenadora de energia. Entre as substâncias liberadas pelo adipócito incluem-se a adiponectina, o fator de necrose tumoral-alfa, a interleucina-6 e a leptina. Especificamente, a leptina desempenha importante papel no controle da ingestão alimentar e no controle do peso corporal em mamíferos. Além disso, o hormônio ghrelina, recentemente descoberto, também parece influenciar o metabolismo energético e a obesidade. As alterações que o exercício físico provoca na fisiologia endócrino-metabólica podem contribuir sobremaneira para a prática clínica. Assim, essa revisão abordará os conhecimentos mais recentes sobre a leptina, a ghrelina e o papel dos diferentes tipos de exercício físico sobre estes hormônios. Os trabalhos mostram que a relação entre o exercício físico e a concentração plasmática desses peptídeos ainda não está clara. As razões para isso poderiam ser devidas aos diferentes protocolos de treinamento físico empregados nos estudos. Além disso, diferenças genéticas também podem explicar as discrepâncias entre os resultados obtidos em seres humanos, pois a existência de polimorfismo em alguns genes pode acarretar respostas celulares diferentes frente ao exercício físico.

O papel dos hormônios leptina e grelina na gênese da obesidade

A prevalência da obesidade está aumentando e estudos prospectivos mostram que, em 2025, o Brasil será o quinto país do mundo a apresentar problemas de obesidade em sua população. A etiologia da obesidade não é de fácil identificação, uma vez que a mesma é caracterizada como uma doença multifatorial, ou seja, diversos fatores estão envolvidos em sua gênese, incluindo fatores genéticos, psicológicos, metabólicos e ambientais. Pesquisas recentes na área de metabolismo mostram que o adipócito é capaz de sintetizar várias substâncias e, diferentemente do que se supunha anteriormente, o tecido adiposo não é apenas um sítio de armazenamento de triglicérides, é hoje considerado um órgão endócrino. Dentre as diversas substâncias sintetizadas pelo adipócito, destacam-se a adiponectina, a angiotensina e a leptina. A leptina é um petídeo que desempenha importante papel na regulação da ingestão alimentar e no gasto energético, gerando um aumento na queima de energia e diminuindo a ingestão alimentar. Além dos avanços no estudo da célula adiposa, um novo hormôrnio relacionado ao metabolismo foi descoberto recentemente, a grelina. A grelina é um peptídeo produzido nas células do estômago, e está diretamente envolvida na regulação do balanço energético a curto prazo. Assim, este artigo abordará o papel da leptina e da grelina no controle do peso corporal e as limitações que ainda existem para tratar a obesidade em humanos.

Polimorfismos no gene do hormônio da grelina (GHRL) e suas associações com características de interesse econômico em bovinos da raça Nelore

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Efeitos do treinamento físico moderado nas concentrações de grelina, leptina e no eixo GH-IGF em ratos diabéticos

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Polimorfismo no gene do hormônio Grelina em búfalas (Bubalus bubalis) e sua associação com produção e qualidade do leite

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Alterações genéticas relacionadas à obesidade: danos no DNA, perfil de expressão e polimorfismos gênicos

Pós-graduação em Patologia - FMB

Gene polymorphisms and increased DNA damage in morbidly obese women

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Growth hormone response to growth hormone-releasing peptide-2 in growth hormone-deficient Little mice

OBJECTIVE: To investigate a possible direct, growth hormone-releasing, hormone-independent action of a growth hormone secretagogue, GHRP-2, in pituitary somatotroph cells in the presence of inactive growth hormone-releasing hormone receptors. MATERIALS AND METHODS: The responses of serum growth hormone to acutely injected growth hormone-releasing P-2 in lit/litmice, which represent a model of GH deficiency arising frommutated growth hormone-releasing hormone-receptors, were compared to those observed in the heterozygous (lit/+) littermates and wild-type (+/+) C57BL/6J mice. RESULTS: After the administration of 10 mcg of growth hormone-releasing P-2 to lit/lit mice, a growth hormone release of 9.3 +/- 1.5 ng/ml was observed compared with 1.04 +/- 1.15 ng/ml in controls (p<0.001). In comparison, an intermediate growth hormone release of 34.5 +/- 9.7 ng/ml and a higher growth hormone release of 163 +/- 46 ng/ml were induced in the lit/+ mice and wild-type mice, respectively. Thus, GHRP-2 stimulated growth hormone in the lit/lit mice, and the release of growth hormone in vivo may be only partially dependent on growth hormone-releasing hormone. Additionally, the plasma leptin and ghrelin levels were evaluated in the lit/lit mice under basal and stimulated conditions. CONCLUSIONS: Here, we have demonstrated that lit/lit mice, which harbor a germline mutation in the Growth hormone-releasing hormone gene, maintain a limited but statistically significant growth hormone elevation after exogenous stimulation with GHRP-2. The present data probably reflect a direct, growth hormone-independent effect on Growth hormone S (ghrelin) stimulation in the remaining pituitary somatotrophs of little mice that is mediated by growth hormone S-R 1a.

Irregular working times and metabolic disorders among truck drivers: a review

A number of studies to better understand the complex physiological mechanism involved in regulating body weight have been conducted. More specifically, the hormones related to appetite, leptin and ghrelin, and their association to obesity have been a focus of investigation. Circadian patterns of these hormones are a new target of research. The behaviour of these hormones in individuals subject to atypical working times such as shiftwork remains unclear. Shiftwork is characterized by changes in biological rhythms and cumulative circadian phase changes, being associated with high rates of obesity and metabolic syndrome. Truck drivers, who work irregular shifts, frequently present a high prevalence of obesity, which might be associated with work-related factors and/or lifestyle. In this context, the aim of this paper was to discuss the relationship of body mass index, appetite-related hormones and sleep characteristics in truck drivers who work irregular shifts compared with day workers.

A modified laparoscopic sleeve gastrectomy for the treatment of diabetes mellitus type 2 and metabolic syndrome in obesity

BACKGROUND: Ghrelin is a gastrointestinal peptide hormone (a 28-amino acid peptide) produced primarily by X/A cells in the oxyntic glands of the stomach fundus and cells lining the duodenum cavern. It suppresses insulin secretion and action and commands a significant role in regulating food intake. The aim of the present study was to show that modified laparoscopic sleeve gastrectomy (MLSG), in which a significant part of the gastric fundus and body of the stomach is removed up to 1 inch from the pylorus vein, may contribute to decreasing circulating ghrelin levels. METHODS: A study population consisting of 150 individuals was monitored after undergoing a MLSG, with individuals chosen based on a documented history of diabetes mellitus type 2 and metabolic syndrome, clinical results determining a body mass index (BMI) of 35 to 60 kg/m(2), peptide C level greater than 1, negative anti-glutamic acid decarboxylase, negative anti-insulin, and confirmed stability of drug/insulin treatment and glycosylated hemoglobin greater than 6.5% for at least 24 and 3 months, respectively, before enrollment. RESULTS: Twenty-four months after surgery, 150 patients (86.6%) presented with normal glycemic levels between 77 and 99 mg/dL. All patients improved average serum insulin levels by 9 mU/L and average glycosylated hemoglobin levels by 5.1% (normal range, 4%-6%). All patients tested negative for Helicobacter pylori and stopped using insulin, with 3 patients prescribed twice-daily use of an oral hypoglycemiant. In 14% of cases, patients experienced partial hair loss with low serum zinc levels and were prescribed oral zinc reposition and topical hair stimulants. The average weight loss recorded was 44.6% for patients with a BMI less than 45 kg/m(2) and 58% for patients with a BMI greater than 50 kg/m(2). CONCLUSIONS: The MLSG is a safe procedure with a low morbidity rate (2.7%) (4 cases of fistula and 2 of bleeding) and no surgical mortality in this study. This surgery can promote control of diabetes mellitus type 2 and aid the treatment of exogenous overweight and morbidly obese individuals. The results of this study show that only through resection of the ghrelin-producing gastric area can most obesity cases and diabetes type II conditions be reverted to nonobese and controlled diabetes. (c) 2012 Elsevier Inc. All rights reserved.

Growth hormone response to growth hormone-releasing peptide-2 in growth hormone-deficient Little mice

OBJECTIVE: To investigate a possible direct, growth hormone-releasing, hormone-independent action of a growth hormone secretagogue, GHRP-2, in pituitary somatotroph cells in the presence of inactive growth hormonereleasing hormone receptors. MATERIALS AND METHODS: The responses of serum growth hormone to acutely injected growth hormone-releasing P-2 in lit/litmice, which represent a model of GH deficiency arising frommutated growth hormone-releasing hormonereceptors, were compared to those observed in the heterozygous (lit/+) littermates and wild-type (+/+) C57BL/6J mice. RESULTS: After the administration of 10 mcg of growth hormone-releasing P-2 to lit/lit mice, a growth hormone release of 9.3±1.5 ng/ml was observed compared with 1.04±1.15 ng/ml in controls (p<0.001). In comparison, an intermediate growth hormone release of 34.5±9.7 ng/ml and a higher growth hormone release of 163±46 ng/ml were induced in the lit/+ mice and wild-type mice, respectively. Thus, GHRP-2 stimulated growth hormone in the lit/lit mice, and the release of growth hormone in vivo may be only partially dependent on growth hormone-releasing hormone. Additionally, the plasma leptin and ghrelin levels were evaluated in the lit/lit mice under basal and stimulated conditions. CONCLUSIONS: Here, we have demonstrated that lit/lit mice, which harbor a germline mutation in the Growth hormone-releasing hormone gene, maintain a limited but statistically significant growth hormone elevation after exogenous stimulation with GHRP-2. The present data probably reflect a direct, growth hormone-independent effect on Growth hormone S (ghrelin) stimulation in the remaining pituitary somatotrophs of little mice that is mediated by growth hormone S-R 1a.