Journal of endocrinology and diabetes最新文献

{"title":"Similar Outcomes for Two Anemia Treatment Strategies among Elderly Hemodialysis Patients with Diabetes.","authors":"M Thamer,&nbsp;Y Zhang,&nbsp;J Kaufman,&nbsp;D Cotter,&nbsp;M A Hernán","doi":"10.15226/2374-6890/1/2/00111","DOIUrl":"https://doi.org/10.15226/2374-6890/1/2/00111","url":null,"abstract":"<p><strong>Background/aims: </strong>To compare mortality and cardiovascular risk in elderly dialysis patients with diabetes under two clinical strategies of anemia correction: maintaining hematocrit (Hct) between 34.5 and < 39.0% (high Hct strategy), and between 30.0 and <34.5% (low Hct strategy) using intravenous alpha epoetin.</p><p><strong>Methods: </strong>Observational data were used to emulate a randomized trial in which diabetic patients who initiated hemodialysis in 2006-2008 were assigned to each anemia correction strategy. Inverse-probability weighting was used to adjust for measured time-dependent confounding.</p><p><strong>Results: </strong>Comparing high with low hematocrit strategy, the hazard ratio (95% confidence interval) was 1.07 (0.83, 1.38) for all-cause mortality and 1.00 (0.81, 1.24) for a composite mortality and cardiovascular endpoint.</p><p><strong>Conclusions: </strong>Among a cohort of elderly hemodialysis patients with diabetes, no differences were found between the low and high hematocrit strategies. A lower target hematocrit - per current Food and Drug Administration (FDA) guidelines - appears to be as safe as higher targets among this population.</p>","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4378694/pdf/nihms649654.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33183526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reproductive Dysfunction from the Stress of Exercise Training is not Gender Specific: The \"Exercise-Hypogonadal Male Condition\".","authors":"Amy R Lane, Anthony C Hackney","doi":"10.15226/2374-6890/1/2/00108","DOIUrl":"10.15226/2374-6890/1/2/00108","url":null,"abstract":"<p><p>Investigative studies point to participation in exercise training as having significant detrimental effects upon reproductive hormonal profiles in men. Specifically, men chronically exposed to training for endurance sports exhibit persistently reduced basal (resting-state) free and total testosterone concentrations without concurrent LH elevations. Men displaying these symptoms have been deemed to exhibit the \"Exercise-Hypogonadal Male Condition\" (EHMC). The exact physiological mechanism inducing the reduction of testosterone in these men is currently unclear, but is postulated to be a dysfunction within the hypothalamic-pituitary-gonadal regulatory axis. The potential exists for the reduced testosterone concentrations within EHMC men to be disruptive and detrimental to some anabolic-androgenic testosterone-dependent physiological processes. Findings, while limited, suggest spermatogenesis problems may exist in some cases; thus, infertility risk in such men is a critical concern. Present evidence suggests the EHMC condition is limited to men who have been persistently involved in chronic endurance exercise training for an extended period of time, and thus is not a highly prevalent occurrence. Nevertheless, it is critical that endocrinologist and fertility clinicians become more aware of the existence of EHMC as a potential problem-diagnosis in their male patients who exercise.</p>","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5897104/pdf/nihms953660.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36012232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary Examination of Olanzapine and Diet Interactions On Metabolism in a Female Macaque.","authors":"Oleg Varlamov,&nbsp;Paul Kievit,&nbsp;Kenny Phu,&nbsp;Arubala P Reddy,&nbsp;Charles T Roberts,&nbsp;Cynthia L Bethea","doi":"10.15226/2374-6890/1/2/00112","DOIUrl":"https://doi.org/10.15226/2374-6890/1/2/00112","url":null,"abstract":"<p><p>Clinical data suggest that atypical antipsychotics such as olanzapine (<b>OLZ</b>) induce significant metabolic changes that are serious side effects of their primary use. Since controlled human studies are problematic and rodent data may be poorly translatable, we have initiated development of a macaque model of OLZ-induced metabolic disease. In this preliminary feasibility study, we examined some metabolic effects of OLZ in a female macaque in the context of a standard low-calorie/fat monkey chow diet followed by a high-fat/sugar Western-style diet (<b>WSD</b>). A female Japanese macaque was administered OLZ (1.25 mg/day) for 6 months, with dietary changes at 2-month intervals as follows: OLZ+Restricted chow, OLZ+Unrestricted chow, OLZ+WSD, and placebo+WSD. Weight was assessed weekly. Glucose tolerance tests (<b>GTT</b>) and Dexascans were performed at baseline and every 2 months. Omental (<b>OM</b>) and subcutaneous (<b>SQ</b>) adipose tissue biopsies were obtained at baseline, after OLZ+Unrestricted chow and after OLZ+WSD to evaluate adipocyte size, lipolysis and insulin-stimulated free fatty acid uptake (<b>FFA</b>). A separate trial was conducted on 2 monkeys with 5 days of OLZ- or no-treatment followed by RT-PCR on rostral and medial basal hypothalamus. Weight increased on OLZ+Restricted chow and stabilized on OLZ+Unrestricted chow. OLZ+WSD did not significantly change the weight plateau. Weight declined upon withdrawal of OLZ with continued WSD. Body fat increased from 14% at baseline to 22%, 30%, 28% and 19% at 2, 4, 6 and 8 mo, respectively, indicating that body fat was elevated on OLZ regardless of diet and declined upon OLZ removal. Glucose tolerance and the insulin response during GTT were normal with OLZ+Restricted chow or OLZ+Unrestricted chow. Addition of WSD with OLZ impaired glucose clearance during GTT. Insulin remained in the normal range, but first phase insulin secretion was reduced. After removal of OLZ, but continued WSD, glucose clearance returned to normal, but this was associated with hyperinsulinemia. Adipocyte diameter was increased in OM and SQ fat by OLZ+chow and OLZ+WSD to a similar extent. (p<0.01, 2-way ANOVA). In OM, isoproterenol-stimulated lipolysis occurred at baseline. In both depots, isoproterenol-stimulated lipolysis occurred with OLZ+chow, but it was significantly blunted by addition of WSD (ANOVA p<0.0001; posthoc p<0.05). Insulin increased FFA uptake at baseline. OLZ +chow or OLZ+WSD increased basal FFA uptake and insulin-induced FFA uptake was blunted in both depots (posthoc p<0.05). There was a marked decrease in POMC gene expression, and increased AgRP and NPY expression in the hypothalamus. There was also a clear increase in serotonin (<b>5HT</b>) 2C, melanocortin (<b>MCR4</b>), and Leptin (<b>LepR</b>) receptor gene expression. These data support the hypotheses that OLZ acts on peripheral tissues as well as in the CNS; that changes in hypothalamic gene expression occur very rapidly and preced","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4301435/pdf/nihms649028.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33003110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of dioxidovanadium (V) complex on cardiovascular metabolism in STZ-induced diabetic male Sprague Dawley rats","authors":"Nombuso Xulu, A. Khathi, Ntethelelo Sibiya, Patrick Mangundu, I. Booysen, P. Ngubane","doi":"10.15226/2374-6890/8/3/001154","DOIUrl":"https://doi.org/10.15226/2374-6890/8/3/001154","url":null,"abstract":"Aims/hypothesis Insulin is an effective hyperglycemia agent, however hyperinsulinemia, as result of prolonged administration, has been shown to lead to cardiovascular disease (CVD) in DM. As a result, research into alternative therapies for the management of diabetes is needed. In our laboratory, a novel vanadium complex has been synthesized and has been shown to improve glycaemic control and liver function. The effects of this complex on cardiovascular metabolism, however, have not yet been established. Therefore, this study sought to investigate the effects of a dioxidovanadium (V) complex on cardiac muscle metabolism in STZ-induced diabetic rats. Vanadium complex was administered twice daily, and blood glucose concentration was monitored for 5 weeks. The animals were sacrificed, blood and hearts were collected for biochemical analysis (western blot (GLUT 1 and 4), pyruvate kinase (PK), acetyl-coA synthetase and ATP synthase) and microscopical analysis (TEM). After 5 weeks, untreated diabetic rats presented with hyperglycaemia compared to non-diabetic rats which was attenuated by vanadium complex administration. The administration of the complex showed an increase in the metabolic activity of enzymes, GLUT 1 and 4 expression. This was further supported by an increased number of mitochondria and their improved structure as shown by transmission electron microscopy. The administration of the dioxidovanadium (V) complex improved cardiovascular metabolism could be a vital hypoglycaemic agent in the management CVD and DM. Keywords: Hyperglycaemia; Vanadium complex; Cardiovascular Metabolism; Diabetes;Hyperlipidaemia.","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67332648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe Gestational Transient Thyrotoxicosis: A Case Report","authors":"B. Shrestha, Chheki Sherpa, R. deBoer, Anita Gabriely","doi":"10.15226/2374-6890/8/2/001153","DOIUrl":"https://doi.org/10.15226/2374-6890/8/2/001153","url":null,"abstract":"We present a case of gestational transient thyrotoxicosis (GTT) associated with hyperemesis gravidarum (HG) highlighting the abnormally elevated free T4 (FT4) found in this instance. This case also highlights that GTT can present as severe and symptomatic hyperthyroidism contrary to its usual presentation of subclinical or mild overt hyperthyroidism. Learning Points 1. Gestational thyrotoxicosis associated with HG can present with severe toxicosis. 2. Symptomatic treatment may be sufficient for the management of this condition. Background One of the etiologies of hyperthyroidism in pregnancy is GTT1. Typically, GTT is a mild, self-limiting condition caused by stimulation of the TSH receptor by human chorionic gonadotropin (hCG).","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67332851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Onset Diabetes and Its Incidence in Severe COVID 19 Disease A Single Centre Study From Kashmir","authors":"A. Parrey, Abir Aijaz, Mohd Ismail, Mir Sadaqat, Murtaza Noor, Yasmeen Amin, Manzoor Koka","doi":"10.15226/2374-6890/8/2/001152","DOIUrl":"https://doi.org/10.15226/2374-6890/8/2/001152","url":null,"abstract":"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that causes coronavirus disease 2019 (COVID-19), was first reported in Wuhan, China, in December 2019 and has spread worldwide. SARS-CoV-2 is a positivestranded RNA virus that is enclosed by a protein containing lipid bilayer with a single-stranded RNA genome; SARS-CoV-2 has 82% homology with human SARS-CoV, which causes severe acute respiratory syndrome.SARS-CoV-2, virus binds to angiotensinconverting enzyme 2 (ACE2) receptors, which are expressed in key metabolic organs and tissues, including pancreatic beta cells, adipose tissue, the small intestine, and the kidneys. Thus, it is believed that SARS-CoV-2 may cause pleiotropic alterations of glucose metabolism that could complicate the pathophysiology of pre-existing diabetes or lead to new mechanisms of disease. Many studies have made observations that provide support for the hypothesis of a potential diabetogenic effect of Covid-19; in addition it is well-recognized that stress response associated with severe illness have diabetogenic effect. However, whether the alterations of glucose metabolism that occur with a sudden onset in severe COVIOD-19 persist or remit when the infection resolves is unclear. How frequent is the phenomenon of newonset diabetes, and is it classic type 1 or type 2 diabetes or a new type of diabetes. Key words: COVID 19; Prediabetes; Diabetes; Pneumonia.","PeriodicalId":73731,"journal":{"name":"Journal of endocrinology and diabetes","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67332684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}