Search Results
You are looking at 41 - 50 of 546 items for
- Abstract: Aging x
- Abstract: Inflammation x
- Abstract: Cognition x
Search for other papers by Sheila Leone in
Google Scholar
PubMed
Search for other papers by Lucia Recinella in
Google Scholar
PubMed
Search for other papers by Annalisa Chiavaroli in
Google Scholar
PubMed
Search for other papers by Claudio Ferrante in
Google Scholar
PubMed
Search for other papers by Giustino Orlando in
Google Scholar
PubMed
Search for other papers by Michele Vacca in
Google Scholar
PubMed
Search for other papers by Roberto Salvatori in
Google Scholar
PubMed
Search for other papers by Luigi Brunetti in
Google Scholar
PubMed
Background
Growth hormone-releasing hormone (GHRH) plays an important role in brain functions. The aim of this study was to examine cognitive functions and emotional behaviour in a mouse model of isolated GH deficiency due to bi-allelic ablation of the GHRH gene (GHRH knockout, GHRHKO).
Methods
Learning, memory and emotional behaviour were evaluated using a series of validated tests (Morris water maze, eight-arm radial maze, open field, elevated plus maze test, forced swim tests) in 2-, 5- and 12-month-old male mice either homozygous (−/−) or heterozygous (+/−) for the GHRHKO allele.
Results
Compared with age-matched +/− mice, −/− mice showed decreased cognitive performance in Morris water maze and eight-arm radial maze tests. By comparing the effects of aging in each genotype, we observed an age-related impairment in test results in +/− mice, while in −/− mice a significant decline in cognitive function was found only in 12 months compared with 2-month-old mice, but no difference was found between 5 months old vs 2 months old. −/− mice showed increased exploration activity compared to age-matched +/− controls, while both strains of mice had an age-related decrease in exploration activity. When evaluated through open field, elevated plus maze and forced swim tests, −/− mice demonstrated a decrease in anxiety and depression-related behaviour compared to age-matched +/− controls.
Conclusions
Our results suggest that homozygous ablation of GHRH gene is associated with decreased performance in learning and memory tests, possibly linked to increased spontaneous locomotor activity. In addition, we observed an age-related decline in cognitive functions in both genotypes.
Department of Child and Adolescent Medicine, Section of Pediatric Cardiology, University Hospital Jena, Am Klinikum, Jena, Germany
Search for other papers by Alexandra Kiess in
Google Scholar
PubMed
Search for other papers by Jessica Green in
Google Scholar
PubMed
Search for other papers by Anja Willenberg in
Google Scholar
PubMed
Search for other papers by Uta Ceglarek in
Google Scholar
PubMed
Search for other papers by Ingo Dähnert in
Google Scholar
PubMed
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany
Search for other papers by Wieland Kiess in
Google Scholar
PubMed
Department of Women and Child Health, Hospital for Children and Adolescents and Center for Pediatric Research (CPL), University of Leipzig, Liebigstrasse, Leipzig, Germany
Search for other papers by Mandy Vogel in
Google Scholar
PubMed
Background and objectives
As part of the LIFE Child study, we previously described the associations between N-terminal-pro-hormone brain natriuretic peptide (NT-proBNP) and hs-troponin T (hs-TnT) levels and an individual’s sex, age and pubertal status, as well as with body mass index (BMI) and serum lipid levels. For NT-proBNP, we found inverse associations with advancing puberty, increasing BMI and serum lipid levels. These findings led us to further question the putative influences of the developing individual’s metabolic and growth status as represented by levels of insulin-like growth factor-1 (IGF-1) and IGF-1-binding protein-3 (IGF-BP3) as well as hemoglobin A1c (HbA1c) and Cystatin C (CysC).
Material and methods
Serum values, medical history and anthropometric data provided by 2522 children aged 0.25–18 years were collected and analyzed as per study protocol.
Results
A strong negative association between NT-proBNP values and IGF-1, IGF-BP3 and HbA1c levels was identified. For IGF-BP3, this interaction was modulated by sex and age, for HbA1c only by age. For hs-TnT, a positive association was found with IGF-BP3, IGF-1 and CysC. The association between hs-TnT and IGF-1 was sex dependent. The association between CysC and hs-TnT was stronger in girls, but the interaction with age was only seen in boys. Between hs-TnT and HbA1c, the association was significantly negative and modulated by age.
Conclusion
Based on our large pediatric cohort, we could identify age- and sex-dependent interactions between the metabolic status represented by IGF-1, IGF-BP3, CysC and HbA1c levels and the cardiac markers NT-proBNP and hs-TnT.
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Search for other papers by Wolfgang Högler in
Google Scholar
PubMed
Search for other papers by Agnès Linglart in
Google Scholar
PubMed
Search for other papers by Anna Petryk in
Google Scholar
PubMed
Search for other papers by Priya S Kishnani in
Google Scholar
PubMed
Search for other papers by Lothar Seefried in
Google Scholar
PubMed
Search for other papers by Shona Fang in
Google Scholar
PubMed
Search for other papers by Cheryl Rockman-Greenberg in
Google Scholar
PubMed
Search for other papers by Keiichi Ozono in
Google Scholar
PubMed
Search for other papers by Kathryn Dahir in
Google Scholar
PubMed
Search for other papers by Gabriel Ángel Martos-Moreno in
Google Scholar
PubMed
Objective
Hypophosphatasia, an inborn error of metabolism characterized by impaired bone mineralization, can affect growth. This study evaluated relationships between anthropometric parameters (height, weight, and body mass index) and clinical manifestations of hypophosphatasia in children.
Design
Data from children (aged <18 years) with hypophosphatasia were analyzed from the observational Global Hypophosphatasia Registry.
Methods
Anthropometric parameters were evaluated by age group (<2 years and ≥2 years) at assessment. The frequency of hypophosphatasia manifestations was compared between children with short stature (< percentile) and those with normal stature.
Results
This analysis included 215 children (54.4% girls). Short stature presented in 16.1% of children aged <2 years and 20.4% of those aged ≥2 years at assessment. Among those with available data (n = 62), height was below the target height (mean: −0.66 standard deviations). Substantial worsening of growth (mean delta height z score: −1.45; delta weight z score: −0.68) occurred before 2 years of age, while in those aged ≥2 years, anthropometric trajectories were maintained (delta height z score: 0.08; delta weight z score: 0.13). Broad-ranging hypophosphatasia manifestations (beyond dental) were observed in most children.
Conclusions
Short stature was not a consistent characteristic of children with hypophosphatasia, but growth impairment was observed in those aged <2 years, indicating that hypophosphatasia might affect growth plate activity during infancy. In addition, a broad range of clinical manifestations occurred in those above and below the third percentile for height, suggesting that height alone may not accurately reflect hypophosphatasia disease burden and that weight is less affected than longitudinal growth.
Department of Paediatric Endocrinology, Gynaecology, and Diabetology, AP-HP, Necker-Enfants Malades University Hospital, IMAGINE Institute affiliate, Paris, France
Search for other papers by Isabelle Flechtner in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Gynaecology, and Diabetology, AP-HP, Necker-Enfants Malades University Hospital, IMAGINE Institute affiliate, Paris, France
Search for other papers by Magali Viaud in
Google Scholar
PubMed
Search for other papers by Dulanjalee Kariyawasam in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Gynaecology, and Diabetology, AP-HP, Necker-Enfants Malades University Hospital, IMAGINE Institute affiliate, Paris, France
Search for other papers by Marie Perrissin-Fabert in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Gynaecology, and Diabetology, AP-HP, Necker-Enfants Malades University Hospital, IMAGINE Institute affiliate, Paris, France
Search for other papers by Maud Bidet in
Google Scholar
PubMed
Department of Endocrinology and Reproductive Medicine, AP-HPIE3M, Hôpital Pitié-Salpêtrière, ICAN, Paris, France
Search for other papers by Anne Bachelot in
Google Scholar
PubMed
Department of Endocrinology and Reproductive Medicine, AP-HPIE3M, Hôpital Pitié-Salpêtrière, ICAN, Paris, France
Search for other papers by Philippe Touraine in
Google Scholar
PubMed
Search for other papers by Philippe Labrune in
Google Scholar
PubMed
Centre for Rare Gynecological Disorders, Hospital Universitaire Necker-Enfants Malades, Paediatric Endocrinology, Gynaecology and Diabetology, AP-HP, Université de Paris, Paris, France
Search for other papers by Pascale de Lonlay in
Google Scholar
PubMed
Department of Paediatric Endocrinology, Gynaecology, and Diabetology, AP-HP, Necker-Enfants Malades University Hospital, IMAGINE Institute affiliate, Paris, France
Centre for Rare Gynecological Disorders, Hospital Universitaire Necker-Enfants Malades, Paediatric Endocrinology, Gynaecology and Diabetology, AP-HP, Université de Paris, Paris, France
Search for other papers by Michel Polak in
Google Scholar
PubMed
Classic galactosemia is a rare inborn error of galactose metabolism with a birth prevalence of about 1/30,000–60,000. Long-term complications occurring despite dietary treatment consist of premature ovarian insufficiency (POI) and neurodevelopmental impairments. We performed with the French Reference Centers for Rare Diseases a multisite collaborative questionnaire survey for classic galactosemic patients. Its primary objective was to assess their puberty, pregnancy, gonadotropic axis, and pelvic morphology by ultrasound. The secondary objective was to determine predictive factors for pregnancy without oocyte donation. Completed questionnaires from 103 patients, 56 females (median age, 19 years (3–52 years)) and 47 males (median age, 19 years (3–45 years)), were analyzed. Among the 43 females older than 13 years old, mean age for breast development first stage was 13.8 years; spontaneous menarche occurred in 21/31 females at a mean age of 14.6 years. In these 21 women, 62% had spaniomenorrhea and 7/17 older than 30 years had amenorrhea. All age-groups confounded, FSH was above reference range for 65.7% of the patients, anti-Müllerian hormone and inhibin B were undetectable, and the ovaries were small with few or no follicles detected. Among the 5 females who sought to conceive, 4 had pregnancies. Among the 47 males, 1 had cryptorchidism, all have normal testicular function and none had a desire to conceive children. Thus, spontaneous puberty and POI are both common in this population. Spontaneous menarche seems to be the best predictive factor for successful spontaneous pregnancy.
Search for other papers by Karim Gariani in
Google Scholar
PubMed
Diabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland
Search for other papers by François R Jornayvaz in
Google Scholar
PubMed
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the industrialized world. NAFLD encompasses a whole spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. The latter can lead to hepatocellular carcinoma. Furthermore, NASH is the most rapidly increasing indication for liver transplantation in western countries and therefore represents a global health issue. The pathophysiology of NASH is complex and includes multiple parallel hits. NASH is notably characterized by steatosis as well as evidence of hepatocyte injury and inflammation, with or without fibrosis. NASH is frequently associated with type 2 diabetes and conditions associated with insulin resistance. Moreover, NASH may also be found in many other endocrine diseases such as polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or glucocorticoid excess, for example. In this review, we will discuss the pathophysiology of NASH associated with different endocrinopathies.
Search for other papers by Nese Cinar in
Google Scholar
PubMed
Search for other papers by Alper Gurlek in
Google Scholar
PubMed
Adipose tissue secretes a variety of active biological substances, called adipocytokines, that act in an autocrine, paracrine, and endocrine manner. They have roles in appetite control, thermogenesis, and thyroid and reproductive functions. All these molecules may lead to local and generalized inflammation, mediating obesity-associated vascular disorders including hypertension, diabetes, atherosclerosis, and insulin resistance. Thyroid dysfunction is associated with changes in body weight, thermogenesis, and energy expenditure. The connections between cardiovascular risk factors such as dyslipidemia, impaired glucose tolerance, insulin resistance, atherosclerosis, and thyroid dysfunction have been reported in several studies. The adipocytokines serve as causative or protective factors in the development of these disorders in the states of thyroid dysfunction. Abnormal levels of adipocytokines (adiponectin (ADP), leptin, resistin, vaspin, and visfatin) in hypo- and hyperthyroidism have been reported with controversial results. This review aims to update the implication of novel adipokines ADP, vaspin, and visfatin in thyroid dysfunction.
Search for other papers by Ruixin Hu in
Google Scholar
PubMed
Search for other papers by Yanting Yuan in
Google Scholar
PubMed
Search for other papers by Chaolong Liu in
Google Scholar
PubMed
Search for other papers by Ji Zhou in
Google Scholar
PubMed
Search for other papers by Lixia Ji in
Google Scholar
PubMed
Search for other papers by Guohui Jiang in
Google Scholar
PubMed
In patients with type 2 diabetes mellitus (T2DM), the intestinal flora is out of balance and accompanied by leaky gut. The flora is characterized by an increase in mucus-degrading bacteria and a decrease in fiber-degrading bacteria. Short-chain fatty acids (SCFAs), as the major fiber-degrading bacteria fermentation, not only ameliorate the leaky gut, but also activate GPR43 to increase the mass of functional pancreatic β-cells and exert anti-inflammation effect. At present, the gut microbiota is considered as the potential target for anti-diabetes drugs, and how to reverse the imbalance of gut microbiota has become a therapeutic strategy for T2DM. This review briefly summarizes the drugs or compounds that have direct or potential therapeutic effects on T2DM by modulating the gut microbiota, including biguanides, isoquinoline alkaloids, stilbene and C7N-aminocyclic alcohols.
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Wenqi Yang in
Google Scholar
PubMed
Search for other papers by Ling Liu in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Yuan Wei in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Chunlu Fang in
Google Scholar
PubMed
Search for other papers by Fu Zhou in
Google Scholar
PubMed
Search for other papers by Jinbao Chen in
Google Scholar
PubMed
Search for other papers by Qinghua Han in
Google Scholar
PubMed
Search for other papers by Meifang Huang in
Google Scholar
PubMed
Search for other papers by Xuan Tan in
Google Scholar
PubMed
Search for other papers by Qiuyue Liu in
Google Scholar
PubMed
Search for other papers by Qiang Pan in
Google Scholar
PubMed
Search for other papers by Lu Zhang in
Google Scholar
PubMed
Search for other papers by Xiaojuan Lei in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Liangming Li in
Google Scholar
PubMed
Objective
The protective effects of exercise against glucose dysmetabolism have been generally reported. However, the mechanism by which exercise improves glucose homeostasis remains poorly understood. The FGF21–adiponectin axis participates in the regulation of glucose metabolism. Elevated levels of FGF21 and decreased levels of adiponectin in obesity indicate FGF21–adiponectin axis dysfunction. Hence, we investigated whether exercise could improve the FGF21–adiponectin axis impairment and ameliorate disturbed glucose metabolism in diet-induced obese mice.
Methods
Eight-week-old C57BL/6J mice were randomly assigned to three groups: low-fat diet control group, high-fat diet group and high-fat diet plus exercise group. Glucose metabolic parameters, the ability of FGF21 to induce adiponectin, FGF21 receptors and co-receptor levels and adipose tissue inflammation were evaluated after 12 weeks of intervention.
Results
Exercise training led to reduced levels of fasting blood glucose and insulin, improved glucose tolerance and better insulin sensitivity in high-fat diet-induced obese mice. Although serum FGF21 levels were not significantly changed, both total and high-molecular-weight adiponectin concentrations were markedly enhanced by exercise. Importantly, exercise protected against high-fat diet-induced impaired ability of FGF21 to stimulate adiponectin secretion. FGF21 co-receptor, β-klotho, as well as receptors, FGFR1 and FGFR2, were upregulated by exercise. We also found that exercise inhibited adipose tissue inflammation, which may contribute to the improvement in the FGF21–adiponectin axis impairment.
Conclusions
Our data indicate exercise protects against high-fat diet-induced FGF21–adiponectin axis impairment, and may thereby exert beneficial effects on glucose metabolism.
Department of Clinical Research, University of Basel, Basel, Switzerland
Search for other papers by Clara Odilia Sailer in
Google Scholar
PubMed
Department of Biomedicine, University of Basel, Basel, Switzerland
Search for other papers by Sophia Julia Wiedemann in
Google Scholar
PubMed
Search for other papers by Konrad Strauss in
Google Scholar
PubMed
Search for other papers by Ingeborg Schnyder in
Google Scholar
PubMed
Medical Department III, Endocrinology, Nephrology, Rheumatology, University Hospital of Leipzig, Leipzig, Germany
Search for other papers by Wiebke Kristin Fenske in
Google Scholar
PubMed
Department of Clinical Research, University of Basel, Basel, Switzerland
Search for other papers by Mirjam Christ-Crain in
Google Scholar
PubMed
Osmotic stimulus or stress results in vasopressin release. Animal and human in vitro studies have shown that inflammatory parameters, such as interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α), increase in parallel in the central nervous system and bronchial, corneal or intestinal epithelial cell lines in response to osmotic stimulus. Whether osmotic stimulus directly causes a systemic inflammatory response in humans is unknown. We therefore investigated the influence of osmotic stimulus on circulatory markers of systemic inflammation in healthy volunteers. In this prospective cohort study, 44 healthy volunteers underwent a standardized test protocol with an osmotic stimulus leading into the hyperosmotic/hypernatremic range (serum sodium ≥150 mmol/L) by hypertonic saline infusion. Copeptin – a marker indicating vasopressin activity – serum sodium and osmolality, plasma IL-8 and TNF-α were measured at baseline and directly after osmotic stimulus. Median (range) serum sodium increased from 141 mmol/L (136, 147) to 151 mmol/L (145, 154) (P < 0.01), serum osmolality increased from 295 mmol/L (281, 306) to 315 mmol/L (304, 325) (P < 0.01). Median (range) copeptin increased from 4.3 pg/L (1.1, 21.4) to 28.8 pg/L (19.9, 43.4) (P < 0.01). Median (range) IL-8 levels showed a trend to decrease from 0.79 pg/mL (0.37, 1.6) to 0.7 pg/mL (0.4, 1.9) (P < 0.09) and TNF-α levels decreased from 0.53 pg/mL (0.11, 1.1) to 0.45 pg/mL (0.12, 0.97) (P < 0.036). Contrary to data obtained in vitro, circulating proinflammatory cytokines tend to or decrease in human plasma after osmotic stimulus. In this study, osmotic stimulus does not increase circulating markers of systemic inflammation.
Search for other papers by Simon Schimmack in
Google Scholar
PubMed
Department of General Surgery, Xiangya Hospital, Central South University, Changsha, China
Department of Burns and Plastic Surgery, The Third Xiangya Hospital, Central South University, Changsha, China
Search for other papers by Yongchao Yang in
Google Scholar
PubMed
Search for other papers by Klaus Felix in
Google Scholar
PubMed
Search for other papers by Markus Herbst in
Google Scholar
PubMed
Search for other papers by Yixiong Li in
Google Scholar
PubMed
Search for other papers by Miriam Schenk in
Google Scholar
PubMed
Search for other papers by Frank Bergmann in
Google Scholar
PubMed
Search for other papers by Thilo Hackert in
Google Scholar
PubMed
Search for other papers by Oliver Strobel in
Google Scholar
PubMed
Objective
Elevated pre-operative C-reactive protein (CRP) serum values have been reported to be associated with poor overall survival for patients with pancreatic neuroendocrine neoplasms (pNEN). The aim of this study was to identify mechanisms linking CRP to poor prognosis in pNEN.
Methods
The malignant properties of pNENs were investigated using the human pNEN cell-lines BON1 and QGP1 exposed to CRP or IL-6. Analyses were performed by ELISA, Western blot, flow cytometry and immunocytochemistry as well as invasion and proliferation assays. To compare cytokine profiles and CRP levels, 76 serum samples of pNEN patients were analyzed using Luminex technology. In parallel, the expression of CRP and growth signaling pathway proteins was assessed on cell lines and paraffin-embedded primary pNEN.
Results
In BON1 and QGP1 cells, inflammation (exposure to IL-6) significantly upregulated CRP expression and secretion as well as migratory properties. CRP stimulation of BON1 cells increased IL-6 secretion and invasion. This was accompanied by activation/phosphorylation of the ERK, AKT and/or STAT3 pathways. Although known CRP receptors – CD16, CD32 and CD64 – were not detected on BON1 cells, CRP uptake of pNEN cells was shown after CRP exposure. In patients, increased pre-operative CRP levels (≥5 mg/L) were associated with significantly higher serum levels of IL-6 and G-CSF, as well as with an increased CRP expression and ERK/AKT/STAT3 phosphorylation in pNEN tissue.
Conclusion
The malignant properties of pNEN cells can be stimulated by CRP and IL-6 promoting ERK/AKT/STAT pathways activation as well as invasion, thus linking systemic inflammation and poor prognosis.
