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Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
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Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
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Absence of leptin confers metabolic dysfunction resulting in morbid obesity. Bone growth and maturation are also impaired. Partial leptin resistance is more common than leptin deficiency and, when induced by feeding mice a high fat diet, often has a negative effect on bone. Here, we used a genetic model to investigate the skeletal effects of partial and total leptin resistance in mice. This was accomplished by comparing the skeletal phenotypes of 17-week-old female C57Bl6/J wild-type (WT) mice, partial leptin receptor-deficient (db/+) mice and leptin receptor-deficient (db/db) mice (n = 7–8/group), all fed a standard diet. Compared to WT mice, db/db mice were dramatically heavier and hyperleptinemic. These mice were also hypogonadal, hyperglycemic, osteopenic and had lower serum levels of bone turnover markers, osteocalcin and C-terminal telopeptide of type I collagen (CTX). Compared to WT mice, db/+ mice were 14% heavier, had 149% more abdominal white adipose tissue, and were mildly hyperglycemic. db/+ mice did not differ from WT mice in uterine weight or serum levels of markers of bone turnover, although there was a trend for lower osteocalcin. At the bone microarchitectural level, db/+ mice differed from WT mice in having more massive femurs and a trend (P = 0.072) for larger vertebrae. These findings suggest that db/+ mice fed a normal mouse diet compensate for partial leptin resistance by increasing white adipose tissue mass which results in higher leptin levels. Our findings suggest that db/+ mice are a useful diet-independent model for studying the effects of partial leptin resistance on the skeleton.
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Insulin-like growth factor 1 (IGF-1) influences bone turnover. Transient decreases in IGF-I levels and/or bioavailability may contribute to the detrimental effects of alcohol on bone. The goals of this non-human primate study were to i) evaluate the 20-h response of bone turnover markers to ethanol consumption and ii) assess how ethanol consumption influences the relationship between IGF-1 and these markers. Osteocalcin (bone formation), carboxyterminal cross-linking telopeptide of type 1 collagen (CTX, bone resorption), IGF-1, and IGF binding protein 1 (IGFBP-1) were measured in plasma from male rhesus macaques (N = 10, 8.4 ± 0.3 years) obtained at 12:00, 16:00, and 06:00 h during two phases: pre-ethanol (alcohol-naïve) and ethanol access. During the ethanol access phase, monkeys consumed 1.5 g/kg/day ethanol (4% w/v) beginning at 10:00 h. Osteocalcin and CTX were lower, and the ratio of osteocalcin to CTX was higher at each time point during ethanol access compared to the pre-ethanol phase. Pre-ethanol marker levels did not vary across time points, but markers varied during ethanol access. IGF-1 levels, but not IGFBP-1 levels, varied during the pre-ethanol phase. In contrast, IGF-1 levels were stable during ethanol access but IGFBP-1 levels varied. There were positive relationships between IGF-1 and turnover markers during the pre-ethanol phase, but not during ethanol access. In conclusion, chronic ethanol consumption reduces levels of bone turnover markers and blocks the normal positive relationship between IGF-1 and turnover markers and alters the normal relationship between IGF-1 and IGFBP-1. These findings support the hypothesis that chronic alcohol consumption leads to growth hormone/IGF-1 resistance.
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Liver production of insulin-like growth factor-I (IGF-I) is a major point of control in the growth hormone (GH)/IGF axis, the endocrine system regulating body growth in fishes and other vertebrates. Pituitary GH stimulates hepatocyte production of IGF-I; however, in catabolic states, hepatocyte GH resistance results in decreases in liver IGF-I production. To investigate endocrine mechanisms leading to the development of hepatocyte GH resistance, we examined the regulation of IGF-I mRNA level by GH and metabolic hormones in primary culture of salmon hepatocytes. Cells were cultured in RPMI medium, and exposed to insulin (Ins, 10−6 M), glucagon (Glu, 10−6 M), triiodothyronine (T3, 10−7 M), dexamethasone (Dex, 10−6 M) and glucagon-like peptide (GLP, 10−6 M), in the presence and absence of GH (5×10−9 M). GH always increased IGF-I mRNA. None of the other hormones tested alone affected IGF-I mRNA. However, Dex, Ins and Glu reduced the response to GH. The response to GH was inhibited by Dex at concentrations of 10−12 M and above, by Ins at 10−9 M and above, and by Glu only at 10−6 M. Inhibition of GH response by glucocorticoids is found in other vertebrates. Salmon hepatocytes were very sensitive to Dex, suggesting that glucocorticoids may play an important role in salmon growth regulation even in unstressed conditions. Inhibition of GH response by Ins is the opposite of what is found in mammals and chickens, suggesting that the role of Ins in growth regulation may differ between fishes and tetrapods. To examine mechanisms for modulation of GH sensitivity, we measured hepatocyte GH receptor (GHR) mRNA levels. Ins inhibited and Dex stimulated GHR mRNA, suggesting that different mechanisms mediate the inhibition of GH response by these hormones. This study shows that glucocorticoids, Ins, and Glu induce GH resistance in cultured salmon hepatocytes.
Metabolism, Diabetes and Obesity Program, Monash Biomedicine Discovery Institute, and Department of Physiology, Monash University, Clayton, Victoria, Australia
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Cathepsin S (CTSS) is a cysteine protease that regulates many physiological processes and is increased in obesity and type 2 diabetes. While previous studies show that deletion of CTSS improves glycaemic control through suppression of hepatic glucose output, little is known about the role of circulating CTSS in regulating glucose and energy metabolism. We assessed the effects of recombinant CTSS on metabolism in cultured hepatocytes, myotubes and adipocytes, and in mice following acute CTSS administration. CTSS improved glucose tolerance in lean mice and this coincided with increased plasma insulin. CTSS reduced G6pc and Pck1 mRNA expression and glucose output from hepatocytes but did not affect glucose metabolism in myotubes or adipocytes. CTSS did not affect insulin secretion from pancreatic β-cells, rather CTSS stimulated glucagon-like peptide (GLP)-1 secretion from intestinal mucosal tissues. CTSS retained its positive effects on glycaemic control in mice injected with the GLP1 receptor antagonist Exendin (9–39) amide. The effects of CTSS on glycaemic control were not retained in high-fat-fed mice or db/db mice, despite the preservation of CTSS’ inhibitory actions on hepatic glucose output in isolated primary hepatocytes. In conclusion, we unveil a role for CTSS in the regulation of glycaemic control via direct effects on hepatocytes, and that these effects on glycaemic control are abrogated in insulin resistant states.
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It is generally accepted that, in mammals, lactotrophs differentiate from somatotrophs through an intermediate cell type, the mammosomatotroph. However, little information exists about mammosomatotrophs and their relationship with lactotroph development in non-mammalian vertebrates. We reported previously that corticosterone (CORT) can induce both somatotroph and lactotroph differentiation in cultures of chicken embryonic pituitary cells. Our current objectives were to determine the abundance of mammosomatotrophs during chicken pituitary development, to identify mammosomatotrophs during CORT induction of lactotrophs, and to explore whether lactotrophs induced by CORT are derived from somatotrophs. Cells that produced prolactin (PRL) only, growth hormone (GH) only or both hormones simultaneously were detected by three approaches – dual immunofluorescence, a combination of immunofluorescence and immunocytochemistry (ICC), and by ICC using combinations of antibodies to GH and PRL. Mammosomatotrophs were not detected between embryonic day (E) 16 and E20, even though lactotrophs increased from nearly absent to greater than 10% of all pituitary cells during this period. CORT induced more than 10% of all E13 pituitary cells to produce PRL, while the percentage of mammosomatotrophs remained at less than 1% of all cells. When cells from the cephalic and caudal lobes of the anterior pituitary were treated separately, CORT increased GH cells in cultures from the caudal lobe. No PRL cells were found in the caudal lobe. In the cephalic lobe, CORT increased lactotrophs, while GH cells were barely detected. In summary, mammosomatotrophs are rare during chicken pituitary development, and CORT does not induce lactotrophs from somatotrophs. These findings indicate that, unlike in mammals, lactotrophs do not differentiate from somatotrophs during chicken embryonic development.
Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand
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Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand
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Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand
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Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand
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Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Department of Oral Biology and Diagnostic Science, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand
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Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand
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using MATLAB program ( Glos et al. 2007 ). A high frequency (HF, 0.6–0.3Hz) was taken as parasympathetic activity, while a low frequency (LF, 0.2–0.6Hz) was taken as a combination of sympathetic and parasympathetic activities ( Chattipakorn et al
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and systems of the progeny. This association has been named programming, which is defined as the basic biological phenomenon that putatively underlies the relationships among nutritional experiences in early life and diseases in adulthood ( Barker 2003
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Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA
Division of Endocrinology, Department of Medicine, Roudebush VA Medical Center and Indiana University School of Medicine, Indianapolis, Indiana, USA
Center for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, Indiana, USA
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. 2003 , 2007 ) and necrosis ( Hoorens et al. 2001 , Scarim et al. 2001 , Fehsel et al. 2003 ). Apoptosis is triggered by intrinsic or extrinsic signals and has classically been considered the lone form of programmed cell death (PCD) ( Alberts
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with pathophysiological consequences ( Pepin et al. 1992 , King et al. 1995 , Reichardt et al. 2000 , Pazirandeh et al. 2002 ). Perinatally, GR levels are programmed to a ‘set point’ by environmental manipulations, including neonatal stress
Biochemistry and Pediatrics, School of Medicine and Biomedical Sciences, Women and Children's Hospital of Buffalo, Departments of
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for immediate survival. However, over the long-term, these adaptations can predispose individuals to the development of the obese phenotype ( Plagemann 2005 ). In the context of the phenomenon of developmental programming, obesity during pregnancy is
