1964-P: Type 1 Diabetes: Sclerostin Resistance Improves Glucose Metabolism and Protects Bone Mass

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1964-P
Author(s):  
GIULIA LEANZA ◽  
YAEL ALIPPE ◽  
SEUNG-YON LEE ◽  
ROCKY STROLLO ◽  
PAOLO POZZILLI ◽  
...  
2011 ◽  
Vol 152 (29) ◽  
pp. 1161-1166 ◽  
Author(s):  
Zsuzsanna Valkusz

Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism. Orv. Hetil., 2011, 152, 1161–1166.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 712-P
Author(s):  
OTHMAR MOSER ◽  
NORBERT J. TRIPOLT ◽  
PETER N. PFERSCHY ◽  
ANNA OBERMAYER ◽  
HARALD KOJZAR ◽  
...  

2017 ◽  
Vol 11 (6) ◽  
pp. 433-435 ◽  
Author(s):  
Nicole D. White

Although fewer individuals with type 1 diabetes mellitus (T1DM) drink alcohol, the potential and severity of harm associated with its consumption is higher in persons with diabetes. Alcohol use affects glucose metabolism and results in various potential adverse effects both from acute ingestion and chronic ingestion in persons with T1DM. The purpose of this article is to describe the effects of alcohol on glucose metabolism and diabetes control in persons with T1DM and propose counseling pearls for providers working with patients in this population.


2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Agnieszka Polkowska ◽  
Izabela Elżbieta Pasierowska ◽  
Marta Pasławska ◽  
Elżbieta Pawluczuk ◽  
Artur Bossowski

Introduction. The increasing knowledge of adropin, afamin, and neudesin and the regulation of glucose metabolism and insulin resistance allows for the assessment of the differences in their concentrations between the groups with varied duration of diabetes mellitus (DM). Aim of the Study. Assessment of serum levels of adropin, afamin, and neudesin in children with type 1 diabetes, with respect to the disease duration. Materials and Methods. The study consisted of 138 patients aged 5–18 years (M 40.58%). Children with type 1 diabetes (n = 68) were compared to the control group (n = 70). The diabetic group was divided into 4 subgroups: (I) newly diagnosed patients, after an episode of ketoacidosis (n = 14), (II) duration no longer than 5 years (n = 18), (III) 5 to 10 years (n = 27), and (IV) longer than 10 years (n = 9). Serum concentrations of adropin, afamin, and neudesin were assessed and compared between the groups of patients. The criterion for statistical significance was p<0.05. Results. The concentrations of adropin and afamin across all subgroups were lower than that in the control group, while neudesin levels were higher in diabetic patients compared to the control group. The differences were statistically significant. Conclusions. Adropin, afamin, and neudesin may play a major role in the regulation of glucose metabolism and have a significant potential as novel biomarkers to predict future metabolic disorders. However, further multicentre studies on a larger cohort of patients are necessary to specify the role of these substances in the course and treatment of type 1 diabetes.


2018 ◽  
Vol 60 (2) ◽  
pp. R57-R75 ◽  
Author(s):  
Heather C Denroche ◽  
C Bruce Verchere

Islet amyloid polypeptide (IAPP), the main component of islet amyloid in type 2 diabetes and islet transplants, is now recognized as a contributor to beta cell dysfunction. Increasingly, evidence warrants its investigation in type 1 diabetes owing to both its immunomodulatory and metabolic actions. Autoreactive T cells to IAPP-derived epitopes have been described in humans, suggesting that IAPP is an islet autoantigen in type 1 diabetes. In addition, although aggregates of IAPP have not been implicated in type 1 diabetes, they are potent pro-inflammatory stimuli to innate immune cells, and thus, could influence autoimmunity. IAPP aggregates also occur rapidly in transplanted islets and likely contribute to islet transplant failure in type 1 diabetes through sterile inflammation. In addition, since type 1 diabetes is a disease of both insulin and IAPP deficiency, clinical trials have examined the potential benefits of IAPP replacement in type 1 diabetes with the injectable IAPP analogue, pramlintide. Pramlintide limits postprandial hyperglycemia by delaying gastric emptying and suppressing hyperglucagonemia, underlining the possible role of IAPP in postprandial glucose metabolism. Here, we review IAPP in the context of type 1 diabetes: from its potential involvement in type 1 diabetes pathogenesis, through its role in glucose metabolism and use of IAPP analogues as therapeutics, to its potential role in clinical islet transplant failure and considerations in this regard for future beta cell replacement strategies.


2018 ◽  
Vol 456 ◽  
pp. 213-223 ◽  
Author(s):  
Rei Kadota ◽  
Kazuma Sugita ◽  
Kenko Uchida ◽  
Hitoshi Yamada ◽  
Masashi Yamashita ◽  
...  

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 110 ◽  
Author(s):  
Gustaf Christoffersson ◽  
Teresa Rodriguez-Calvo ◽  
Matthias von Herrath

Type 1 diabetes is a multifactorial disease in which genetic and environmental factors play a key role. The triggering event is still obscure, and so are many of the immune events that follow. In this brief review, we discuss the possible role of potential environmental factors and which triggers are believed to have a role in the disease. In addition, as the disease evolves, beta cells are lost and this occurs in a very heterogeneous fashion. Our knowledge of how beta cell mass declines and our view of the disease’s pathogenesis are also debated. We highlight the major hallmarks of disease, among which are MHC-I (major histocompatibility complex class I) expression and insulitis. The dependence versus independence of antigen for the immune infiltrate is also discussed, as both the influence from bystander T cells and the formation of neo-epitopes through post-translational modifications are thought to influence the course of the disease. As human studies are proliferating, our understanding of the disease’s pathogenesis will increase exponentially. This article aims to shed light on some of the burning questions in type 1 diabetes research.


2011 ◽  
Vol 20 (4) ◽  
pp. 73-80 ◽  
Author(s):  
Akiko Nishimura ◽  
Kisho Kobayashi ◽  
Hideaki Yagasaki ◽  
Tomohiro Saito ◽  
Kenjiro Nagamine ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document