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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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It is well known that thyroid hormone affects body composition; however, the effect of the thyroid hormone receptor β (TRβ)-selective thyromimetic GC-1 on this biological feature had not been demonstrated. In the current study, we compared the effects of a 6-week treatment with triiodothyronine (T3; daily injections of 3 or 6 μg/100 g body weight) or GC-1 (equimolar doses) on different metabolic parameters in adult female rats. Whereas all animals gained weight (17–25 g) in a way not basically affected by T3 or GC-1 treatment, only T3 treatment selectively increased food intake (50–70%). Oxygen consumption was significantly and equally increased (50–70%) by T3 and GC-1. Analysis of body composition by dual-energy X-ray absorptiometry (DEXA) revealed that, whereas control animals gained about 80% of fat mass, T3- or GC-1-treated animals lost 70–90 and ~20% respectively. Direct analysis of the carcass showed that T3 treatment promoted a 14–74% decrease in fat content but GC-1 treatment promoted only a 15–23% reduction. The gain in lean mass by DEXA and the carcass protein content were not affected by T3 or GC-1 treatment. However, the mass of individual skeletal muscles was negatively affected by T3 but only barely by GC-1. These findings highlight the potential use of GC-1 for the treatment of obesity and the metabolic syndrome.
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Prion diseases are fatal neurodegenerative diseases that can induce endocrinopathies. The basis of altered endocrine function in prion diseases is not well understood, and the purpose of this study was to investigate the spatiotemporal relationship between energy homeostasis and prion infection in hamsters inoculated with either the 139H strain of scrapie agent, which induces preclinical weight gain, or the HY strain of transmissible mink encephalopathy (TME), which induces clinical weight loss. Temporal changes in body weight, feed, and water intake were measured as well as both non-fasted and fasted concentrations of serum glucose, insulin, glucagon, β-ketones, and leptin. In 139H scrapie-infected hamsters, polydipsia, hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia were found at preclinical stages and are consistent with an anabolic syndrome that has similarities to type II diabetes mellitus and/or metabolic syndrome X. In HY TME-infected hamsters, hypodipsia, hypersecretion of glucagon (in both non-fasted and fasted states), increased fasted β-ketones, fasted hypoglycemia, and suppressed non-fasted leptin concentrations were found while feed intake was normal. These findings suggest a severe catabolic syndrome in HY TME infection mediated by chronic increases in glucagon secretion. In both models, alterations of pancreatic endocrine function were not associated with PrPSc deposition in the pancreas. The results indicate that prominent endocrinopathy underlies alterations in body weight, pancreatic endocrine function, and intake of food. The prion-induced alterations of energy homeostasis in 139H scrapie- or HY TME-infected hamsters could occur within areas of the hypothalamus that control food satiety and/or within autonomic centers that provide neural outflow to the pancreas.
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The discovery of a link between an adverse in utero environment and the propensity to develop metabolic and cardiovascular disease in adult life is one of the most important advances in epidemiological research of recent Years. Increasing experimental evidence suggests that alterations in the fetal environment may have long-term consequences for the development of metabolic disorders in adult life. This process has been termed 'fetal programming' and we have shown that undernutrition of the mother during gestation leads to development of the metabolic syndrome X during adult life. Striking metabolic similarities exist between syndrome X and untreated GH deficiency (GHD). In the present study we have investigated the effects of GH treatment on blood pressure and metabolic parameters. Virgin Wistar rats (age 75+/-5 days, n=20 per group) were time-mated and randomly assigned to receive food either ad libitum (AD) or 30% of AD intake (UN) throughout pregnancy. At weaning, male offspring were assigned to one of two diets (control or hypercaloric (30% fat)). Systolic blood pressure was measured at day 100 and following twice daily treatment with recombinant bovine GH for 21 days. GH treatment increased body weights in all treated animals but significantly reduced retroperitoneal and gonadal fat pad weights. Following GH treatment, systolic blood pressure was markedly decreased in all UN offspring. Saline-treated animals showed no change in systolic blood pressure over the treatment period. GH treatment increased heart-to-body weight ratio in all GH-treated animals. Our data demonstrated that GH treatment reduces hypertension and improves cardiovascular function in animals exposed to adverse environmental conditions during fetal or postnatal life.
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Weight reduction is recommended for the treatment of subjects with insulin resistance (IR) syndrome; however, the relative importance of the decrease in body fat or the negative energy balance achieved during a hypo-energetic diet in the improvement of this metabolic syndrome is still debated. Therefore, we undertook to study their relative impact on amelioration of the metabolic abnormalities associated with IR in obese subjects. Twelve obese subjects (six males and six females, mean+/-s.d. body mass index 36.1+/-4.7 kg/m(2)) aged 38-57 years were investigated. During the first phase they were fed a hypo-energetic diet for 6 weeks (week 0-6). During the second phase, lasting 4 weeks (week 6-10) they consumed an iso-energetic diet. During the third phase (week 10-16) the subjects were put again on a hypo-energetic diet. Insulin sensitivity (SI) was assessed by an insulin-enhanced, frequently sampled i.v. glucose tolerance test with minimal model analysis. All subjects reduced weight during both hypo-energetic periods: 5.49+/-0.75 and 2.32+/-0.37%, means+/-s.e.m., P<0.005, week 0-6 and 10-16 respectively. One-third of this loss was achieved within the first week of each period. SI increased by 353+/-121 and 147+/-38% (P<0.005), means+/-s.e.m., at the end of both hypo-energetic periods (week 6 vs 0 and 16 vs 10 respectively). Two-thirds of this improvement were observed within the first week of each period (week 1 vs 0 and 11 vs 10 respectively). During the iso-energetic weight-maintaining period (week 10 vs 6), SI decreased by 43.5+/-7.9% (P<0.002). Serum levels of leptin and triglyceride followed a similar pattern, but to a lesser extent. It may be concluded that negative energy balance is more effective when compared with maintaining a stable lower weight in achieving an improvement in the metabolic parameters of the IR syndrome.
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activates aldosterone/MR signaling involved with metabolic syndrome pathways ( Baudrand et al. 2016 ). Importantly, these findings were not driven by obesity, as the Cav-1 −/− mouse model is known to be lean, and Cav-1 deficiency in humans is associated
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1 blockade influenced the biochemical parameters of metabolic syndrome and systemic insulin resistance. At 2 weeks, mean FPG was 51% greater in OLETF compared to LETO, and ARB had no significant effect. At 11 weeks, mean FPG was 63% higher in OLETF
Department of Regulation Biology, Saitama University, Saitama 378-8570, Japan
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Department of Regulation Biology, Saitama University, Saitama 378-8570, Japan
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Department of Regulation Biology, Saitama University, Saitama 378-8570, Japan
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Introduction Obesity forms a fundamental basis of the metabolic syndrome that involves hyperglycemia, hypertension and hyperlipidemia ( Wajchenberg 2000 , Weiss et al. 2004 , Eckel et al. 2005 ) and is strongly associated with
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an important link between excessive adipose tissue (particularly in the visceral depots) in obesity and associated metabolic syndrome, type 2 diabetes and cardiovascular disease. The three thematic reviews in this issue of the Journal provide a timely
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failure Among the risk factors for HF, we identified the so-called metabolic syndrome, which encompasses multiple metabolic disorders, including high blood pressure, dyslipidaemia, insulin resistance and obesity ( Wang et al . 2010 ). Specifically, both
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Department of Biological Engineering, Division of Comparative Medicine
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Introduction The incidence of obesity and its comorbidities – most notably metabolic syndrome, type 2 diabetes (T2D) and cardiovascular disease (CVD) – continues to increase in both adults and adolescents ( Rosenbaum et al . 2004 ). Metabolic
