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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
DZD (German Center for Diabetes Research), Greifswald, Germany
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Institute and Policlinic for Radiology and Interventional Radiology, University Hospital, Carl-Gustav-Carus University Dresden, Dresden, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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DZHK (German Centre for Cardiovascular Research), Greifswald, Germany
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identified as potential risk factors for fat accumulation in the liver ( 2 ). Therefore, hepatic steatosis is viewed as the hepatic manifestation of the metabolic syndrome ( 3 ). Previous research in obesity and its metabolic consequences has mainly focused
Department of Nuclear Medicine, CHU de Bordeaux, Pessac, France
INRA, Nutrition et Neurobiologie Intégrée, UMR1286, Bordeaux, France
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INRA, Nutrition et Neurobiologie Intégrée, UMR1286, Bordeaux, France
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Department of Nuclear Medicine, CHU de Bordeaux, Pessac, France
INRA, Nutrition et Neurobiologie Intégrée, UMR1286, Bordeaux, France
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Vitamin A (retinol) is a micronutrient critical for cell proliferation and differentiation. In adults, vitamin A and metabolites such as retinoic acid (RA) play major roles in vision, immune and brain functions and tissue remodelling and metabolism. This review presents the physiological interactions of retinoids and endocrine tissues and hormonal systems. Two endocrine systems have been particularly studied. In the pituitary, retinoids target the corticotrophs with a possible therapeutic use in corticotropinomas. In the thyroid, retinoids interfere with iodine metabolism and vitamin A deficiency aggravates thyroid dysfunction caused by iodine-deficient diets. Retinoids use in thyroid cancer appears less promising than expected. Recent and still controversial studies investigated the relations between retinoids and metabolic syndrome. Indeed, retinoids contribute to pancreatic development and modify fat and glucose metabolism. However, more detailed studies are needed before planning any therapeutic use. Finally, retinoids probably play more minor roles in adrenal and gonads development and function apart from their major effects on spermatogenesis.
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Aims/hypothesis
The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low-grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as a result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aim of this study was to investigate if low-grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner.
Methods
We studied eight male hypopituitary patients and eight age- and gender-matched healthy controls during intravenous low-dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360-min infusion with saline and low-dose LPS in each leg respectively.
Results:
Systemic low-grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65 ± 0.51 mg/L (placebo) to 1.92 ± 0.46 mg/L (LPS) at 220 min, P = 0.005 and from 1.66 ± 0.42 mg/L (placebo) to 2.19 ± 0.56 mg/L (LPS) at 340 min, P = 0.006. A very similar response was observed in hypopituitary patients: from 1.59 ± 0.53 mg/L (placebo) to 1.83 ± 0.45 mg/L (LPS) at 220 min, P = 0.021 and from 1.52 ± 0.53 mg/L (placebo) to 2.03 ± 0.44 mg/L (LPS) at 340 min, P < 0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163.
Conclusion:
Systemic low-grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.
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Department of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland
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Objective
To study the use of hormone therapy (HT), morbidity and reproductive outcomes of women with primary ovarian insufficiency (POI) due to FSH-resistant ovaries (FSHRO).
Design
A prospective follow-up study in a university-based tertiary clinic setting.
Methods
Twenty-six women with an inactivating A189V FSH receptor mutation were investigated by means of a health questionnaire and clinical examination. Twenty-two returned the health questionnaire and 14 were clinically examined. Main outcome measures in the health questionnaire were reported as HT, morbidity, medication and infertility treatment outcomes. In the clinical study, risk factors for cardiovascular disease (CVD) and metabolic syndrome (MetS) were compared to age-matched controls from a national population survey (FINRISK). Average number of controls was 326 per FSHRO subject (range 178–430). Bone mineral density and whole-body composition were analyzed with DXA. Psychological and sexual well-being was assessed with Beck Depression Inventory (BDI21), Generalized Anxiety Disorder 7 (GAD-7) and Female Sexual Function Index (FSFI) questionnaires.
Results
HT was initiated late (median 18 years of age) compared with normal puberty and the median time of use was shorter (20–22 years) than the normal fertile period. Osteopenia was detected in 9/14 of the FSHRO women despite HT. No major risk factors for CVD or diabetes were found.
Conclusions
HT of 20 years seems to be associated with a similar cardiovascular and metabolic risk factor profile as in the population control group. However, optimal bone health may require an early-onset and longer period of HT, which would better correspond to the natural fertile period.
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Betty and Guy Beatty Center for Integrated Research, Inova Health System, Falls Church, Virginia, USA
Inova Medicine, Inova Health System, Falls Church, Virginia, USA
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recognized as a liver complication of visceral obesity and other components of metabolic syndrome such as insulin resistance, diabetes, hypertension, and hyperlipidemia ( 3 ). In fact, NAFLD has recently been recognized as the most common cause of chronic
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Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden
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-analysis conducted in 2014 ( 6 ), low SHBG in men was a strong predictor for both prevalent and incident metabolic syndrome, a state that includes alterations in the glucose metabolism and is associated with a five-fold increase in risk for type 2 diabetes mellitus
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, 20 ). Similar findings but with an inverse relationship have also been proposed in men. Approximately one-third of men with T2DM or metabolic syndrome showed subnormal total and free testosterone levels mainly associated with inappropriately low LH
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Global Health Research Institute, School of Human Development and Health, University of Southampton, Southampton, UK
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and s.c. adipose tissue were measured according to previously described methodology ( 17 ). Blood analyte assays and diagnosis of the metabolic syndrome and menopause staging Fasting blood samples were obtained in the morning before 11:00 h
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-/amenorrhea. Besides the clinical features of hyperandrogenism (hirsutism, acne, male-type baldness), oligo-/amenorrhea and impaired fertility, PCOS patients are often insulin resistant, obese and have metabolic syndrome, with arterial hypertension, dyslipidemia
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Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden
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studies that support the hypothesis that low testosterone levels in men increase the risk for developing diabetes and the metabolic syndrome. Both the NHANES III-study and the Massachusetts Male aging study found an increased risk of type 2 diabetes and
