Journal of endocrinology, diabetes & obesity最新文献

Effects of Three Low-Doses of D-Tagatose on Glycemic Control Over Six Months in Subjects with Mild Type 2 Diabetes Mellitus Under Control with Diet and Exercise. 三种低剂量d -塔格糖在饮食和运动控制下对轻度2型糖尿病患者6个月血糖控制的影响

Journal of endocrinology, diabetes & obesity Pub Date : 2014-10-01

Mark Ensor, Jarrod Williams, Rebecca Smith, Amy Banfield, Robert A Lodder

{"title":"Effects of Three Low-Doses of D-Tagatose on Glycemic Control Over Six Months in Subjects with Mild Type 2 Diabetes Mellitus Under Control with Diet and Exercise.","authors":"Mark Ensor, Jarrod Williams, Rebecca Smith, Amy Banfield, Robert A Lodder","doi":"","DOIUrl":"","url":null,"abstract":"The primary objective of this study was to evaluate the safety and the effect of D-tagatose on the glycemic control of subjects with type 2 diabetes as determined by HbA1c levels at the end of 6 months of therapy using the subject's own baseline HbA1c level as a comparator. The determination of the minimal dose required to cause a statistically significant reduction in HbA1c was of particular interest. Eight weeks after screening, the qualifying subjects were randomized to receive one of three doses of D-tagatose: 2.5 g TID, 5.0 g TID or 7.5 g TID. Blood levels of HbA1c, fasting blood glucose concentrations, plasma lipids, changes in body weight, changes in body mass index, and change in insulin levels were checked at each study visit and at the end of the study. Treatment success, as measured by the reduction of HbA1c, was greatest for the 7.5 g D-tagatose dose group, although the difference between the treatments was not statistically significant. For fasting glucose, only the 7.5 g dosage group exhibited reductions from baseline at the 3- and 6-month time points. Mean body weights reduced in a dose-response fashion, with the 5.0 g and the 7.5 g D-tagatose doses providing the greatest reductions. D-tagatose at dosages of 2.5 g, 5.0 g, and 7.5 g TID for six months were well tolerated by this subject population. D-tagatose at 5.0 g TID was the minimal dose required to reduce HbA1c. D-tagatose at 7.5 g TID provided the greatest effect in most measured efficacy parameters.","PeriodicalId":90592,"journal":{"name":"Journal of endocrinology, diabetes & obesity","volume":"2 4","pages":"1057"},"PeriodicalIF":0.0,"publicationDate":"2014-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287278/pdf/nihms643060.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32968630","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}

引用次数: 0

Thyroid Hormone Signaling in Muscle Development, Repair and Metabolism. 甲状腺激素信号在肌肉发育、修复和代谢中的作用。

Journal of endocrinology, diabetes & obesity Pub Date : 2014-07-01

Jang-Won Lee, Nam-Ho Kim, Anna Milanesi

引用次数: 0

TRANSCRIPTION FACTOR GLI-SIMILAR 3 (GLIS3): IMPLICATIONS FOR THE DEVELOPMENT OF CONGENITAL HYPOTHYROIDISM. 转录因子glis3 (glis3)：与先天性甲状腺功能减退症的发展有关。

Journal of endocrinology, diabetes & obesity Pub Date : 2014-04-01

Kristin Lichti-Kaiser, Gary ZeRuth, Anton M Jetten

{"title":"TRANSCRIPTION FACTOR GLI-SIMILAR 3 (GLIS3): IMPLICATIONS FOR THE DEVELOPMENT OF CONGENITAL HYPOTHYROIDISM.","authors":"Kristin Lichti-Kaiser, Gary ZeRuth, Anton M Jetten","doi":"","DOIUrl":"","url":null,"abstract":"Congenital hypothyroidism (CH) is the most frequent endocrine disorder in neonates. While several genetic mutations have been identified that result in developmental defects of the thyroid gland or thyroid hormone synthesis, genetic factors have yet to be identified in many CH patients along with the mechanisms underlying their pathophysiology. Mutations in the gene encoding the Krüppel-like transcription factor, GLI-similar 3 (GLIS3) have been associated with the development of a syndrome characterized by congenital hypothyroidism and neonatal diabetes and similar phenotypes were observed in mouse knockout models of Glis3. Patients with GLIS3-mediated CH exhibit diminished serum levels of thyroxine (T4) and triiodothyronine (T3) and elevated thyroid stimulating hormone (TSH) and thyroglobulin (TG). However, the inconsistent presentation of clinical features associated with this CH has made it difficult to ascertain a causative mechanism. Future elucidation of the biological functions of GLIS3 in the thyroid will be crucial to the discovery of new therapeutic opportunities for the treatment of CH.","PeriodicalId":90592,"journal":{"name":"Journal of endocrinology, diabetes & obesity","volume":"2 2","pages":"1024"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4131692/pdf/nihms-610593.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32593442","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}

引用次数: 0

Pancreatic and Islet Development and Function: The Role of Thyroid Hormone. 胰腺和胰岛的发育和功能:甲状腺激素的作用。

Journal of endocrinology, diabetes & obesity Pub Date : 2014-01-01

Teresa L Mastracci, Carmella Evans-Molina

引用次数: 0

Frailty Attenuates the Impact of Metformin on Reducing Mortality in Older Adults with Type 2 Diabetes. 虚弱减弱二甲双胍对降低老年2型糖尿病患者死亡率的影响。

Journal of endocrinology, diabetes & obesity Pub Date : 2014-01-01

Chen-Pin Wang, Carlos Lorenzo, Sara E Espinoza

{"title":"Frailty Attenuates the Impact of Metformin on Reducing Mortality in Older Adults with Type 2 Diabetes.","authors":"Chen-Pin Wang, Carlos Lorenzo, Sara E Espinoza","doi":"","DOIUrl":"","url":null,"abstract":"Objective: To determine whether the protective effect of metformin against death is modified by frailty status in older adults with type 2 diabetes.Research design and methods: We conducted a cohort study during October 1, 1999-September 30, 2006 among veterans aged 65-89 years old with type 2 diabetes but without history of liver, renal diseases, or cancers, who had sulfonylureas or metformin as the sole antidiabetic drug for ≥180 days. The Cox proportional hazard model was used to compare hazard rates of all-cause mortality between the metformin and sulfonylurea users adjusting for the propensity score of metformin use and covariates: age, race/ethnicity, diabetes duration, Charlson comorbidity score, statin use, smoking status, BMI, LDL, and HbA1c.Results: In this cohort of 2,415 veterans, 307 (12.7%) were metformin users, 2,108 (87.3%) were sulfonylurea users, the mean age was 73.7±5.2 years, the mean study period was 5.6±2.3 years, the mean HbA1c at baseline was 6.7±1.0%, 23% had diabetes for ≥10 years, and 43.6% (N=1,048) died during the study period. For patients with and without frailty, the adjusted hazard ratio (HR) of death for metformin vs. sulfonylurea use were 0.92 (95% CI=0.90-1.31, p-value=0.19) and 0.69 (95% CI = 0.60-0.79, p-value<0.001), respectively. Logistic regression analyses showed that metformin (vs. sulfonylurea) was significantly associated with a decreased odds of frailty (OR: 0.66, 95% CI: 0.61-0.71, p-value <.0001).Conclusion: Our study suggests that metformin could potentially promote longevity via preventing frailty in older adults with type 2 diabetes.","PeriodicalId":90592,"journal":{"name":"Journal of endocrinology, diabetes & obesity","volume":"2 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/PMC4264048/pdf/nihms608636.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32907377","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}

引用次数: 0

The EP3 Receptor: Exploring a New Target for Type 2 Diabetes Therapeutics. EP3受体:探索2型糖尿病治疗的新靶点

Journal of endocrinology, diabetes & obesity Pub Date : 2013-07-01

Joshua C Neuman, Michelle E Kimple

引用次数: 0

Nutrient Excess in AMPK Downregulation and Insulin Resistance. 营养过剩导致 AMPK 下调和胰岛素抵抗。

Journal of endocrinology, diabetes & obesity Pub Date : 2013-07-01

Kimberly A Coughlan, Rudy J Valentine, Neil B Ruderman, Asish K Saha

{"title":"Nutrient Excess in AMPK Downregulation and Insulin Resistance.","authors":"Kimberly A Coughlan, Rudy J Valentine, Neil B Ruderman, Asish K Saha","doi":"","DOIUrl":"","url":null,"abstract":"It is well established that chronic exposure to excess nutrients leads to insulin resistance (IR) in skeletal muscle. Since skeletal muscle is responsible for 70-80% of insulin-stimulated glucose uptake, skeletal muscle IR is a key pathological component of type 2 diabetes (T2D). Recent evidence suggests that inhibition of the nutrient-sensing enzyme AMP-activated protein kinase (AMPK) is an early event in the development of IR in response to high glucose, branched chain amino acids (BCAA), or fatty acids (FA). Whether the decrease in AMPK activity is causal to the events leading to insulin resistance (increased mTOR/p70S6K signaling) remains to be determined. Interestingly, pharmacological activation of AMPK can prevent activation of mTOR/p70S6K and insulin resistance, while inhibition of mTOR with rapamycin prevents insulin resistance, but not AMPK downregulation. AMPK can be inhibited by increased energy state (reduced AMP/ATP ratio), decreased phosphorylation of its activation site (αThr172) (by decreased upstream kinase activity or increased phosphatase activity), increased inhibitory phosphorylation at αSer485/491, changes in redox state or hormone levels, or other yet to be identified mechanisms. Excess nutrients also lead to an accumulation of the toxic lipid intermediates diacylglycerol (DAG) and ceramides, both of which can activate various protein kinase C (PKC) isoforms, and contribute to IR. The mechanism responsible for the initial downregulation of AMPK in response to excess nutrients, and whether glucose, BCAA, and FA act through similar or different pathways requires further study. Identification of this mechanism and the relative importance of other events would be beneficial for designing novel pharmacological interventions to prevent and/or reverse IR. This review will focus on the some of the mechanisms responsible for AMPK downregulation and the relative sequence and importance of these events.","PeriodicalId":90592,"journal":{"name":"Journal of endocrinology, diabetes & obesity","volume":"1 1","pages":"1008"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479300/pdf/nihms-686825.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33303080","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}

引用次数: 0