scholarly journals Altered bone mass, geometry and mechanical properties during the development and progression of type 2 diabetes in the Zucker diabetic fatty rat

2008 ◽  
Vol 199 (3) ◽  
pp. 379-388 ◽  
Author(s):  
Rhonda D Prisby ◽  
Joshua M Swift ◽  
Susan A Bloomfield ◽  
Harry A Hogan ◽  
Michael D Delp

Osteopenia and an enhanced risk of fracture often accompany type 1 diabetes. However, the association between type 2 diabetes and bone mass has been ambiguous with reports of enhanced, reduced, or similar bone mineral densities (BMDs) when compared with healthy individuals. Recently, studies have also associated type 2 diabetes with increased fracture risk even in the presence of higher BMDs. To determine the temporal relationship between type 2 diabetes and bone remodeling structural and mechanical properties at various bone sites were analyzed during pre-diabetes (7 weeks), short-term (13 weeks), and long-term (20 weeks) type 2 diabetes. BMDs and bone strength were measured in the femora and tibiae of Zucker diabetic fatty rats, a model of human type 2 diabetes. Increased BMDs (9–10%) were observed in the distal femora, proximal tibiae, and tibial mid- shafts in the pre-diabetic condition that corresponded with higher plasma insulin levels. During short- and long-term type 2 diabetes, various parameters of bone strength and BMDs were lower (9–26%) in the femoral neck, distal femora, proximal tibiae, and femoral and tibial mid-shafts. Correspondingly, blood glucose levels increased by 125% and 153% during short- and long-term diabetes respectively. These data indicate that alterations in BMDs and bone mechanical properties are closely associated with the onset of hyperinsulinemia and hyperglycemia, which may have direct adverse effects on skeletal tissue. Consequently, disparities in the human literature regarding the effects of type 2 diabetes on skeletal properties may be associated with the bone sites studied and the severity or duration of the disease in the patient population studied.

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Amanda L. Missel ◽  
Laura R. Saslow ◽  
Dina H. Griauzde ◽  
Donna Marvicsin ◽  
Ananda Sen ◽  
...  

Abstract Introduction Chronic inflammation is associated with the development, progression and long-term complications of type 2 diabetes. Hyperglycemia is associated with chronic low-grade inflammation, and thus has become the focus of many screening and treatment recommendations. We hypothesize that insulin may also be associated with inflammation and may be an additional factor to consider in screening and treatment. Methods This study used National Health and Nutrition Examination Survey data from 2005 to 2010 to analyze the association between fasting insulin and C-reactive protein (CRP). A two-part model was used due to the high number of values reported as 0.1 mg/L. Two models were analyzed, both with and without the addition of waist circumference to other covariates in the model. Results The final sample included 4527 adults with a mean age of 43.31 years. In the first model, higher fasting insulin was associated with increased odds of CRP > 0.1 mg/L (OR = 1.02, p < .001) and with higher CRP (β = 0.03, p < .001). In the adjusted model, including waist circumference as a covariate, higher fasting insulin was not associated with CRP > 0.1 mg/L (OR = 1.00, p = .307) but the association between higher fasting insulin and higher continuous CRP remained significant (β = 0.01, p = .012). Conclusion This study found that higher fasting insulin is associated with higher CRP. These results suggest that treatment approaches that simultaneously decrease insulin levels as well as glucose levels may provide additive anti-inflammatory effects, and therefore may improve long-term outcomes for adults with type 2 diabetes.


2013 ◽  
Vol 16 (3) ◽  
pp. A164
Author(s):  
P.D. Home ◽  
G.G. Gálvez ◽  
R. Malek ◽  
E. Hammerby ◽  
A. Nikolajsen ◽  
...  

2016 ◽  
Vol 26 (10) ◽  
pp. 2442-2448 ◽  
Author(s):  
Gian Franco Adami ◽  
Raffaella Gradaschi ◽  
Gabriella Andraghetti ◽  
Nicola Scopinaro ◽  
Renzo Cordera

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2074 ◽  
Author(s):  
Pedram Shokouh ◽  
Per B Jeppesen ◽  
Christine B Christiansen ◽  
Fredrik B Mellbye ◽  
Kjeld Hermansen ◽  
...  

The effects of chronic coffee exposure in models of type 2 diabetes mellitus (T2D) models is scarcely studied, and the efficacy of the main coffee species has never been compared. We tested the hypothesis that long-term consumption of arabica and robusta coffee may differentially delay and affect T2D development in Zucker diabetic fatty rats. Three study groups received either chow mixed with arabica or robusta instant coffee (1.8% w/w) or unsupplemented chow food for 10 weeks. Both coffee species reduced liver triglyceride content and area under the curve of fasting and postprandial insulin. At study end, plasma adiponectin, total cholesterol and high density lipoprotein levels were higher in the robust group compared with both arabica and control groups. The liver gene expression of Glucose-6-phosphatase, catalytic subunit (G6pc) and Mechanistic target of rapamycin (mTOR) in robusta and Cpt1a in both coffee groups was downregulated. In conclusion, long-term consumption of both coffee species reduced weight gain and liver steatosis and improved insulin sensitivity in a rat model of T2D. Robusta coffee was seemingly superior to arabica coffee with respect to effects on lipid profile, adiponectin level and hepatic gene expression.


2017 ◽  
Vol 22 (44) ◽  
pp. 6716-6721 ◽  
Author(s):  
Giordana Maluf da Silva ◽  
Katia Camarano Nogueira ◽  
Rosa Tsuneshiro Fukui ◽  
Marcia Regina Soares Correia ◽  
Rosa Ferreira dos Santos ◽  
...  

2013 ◽  
Vol 28 (3) ◽  
pp. 627-638 ◽  
Author(s):  
Christine Hamann ◽  
Martina Rauner ◽  
Yvonne Höhna ◽  
Ricardo Bernhardt ◽  
Jan Mettelsiefen ◽  
...  

2015 ◽  
Vol 22 (2) ◽  
pp. 201-207 ◽  
Author(s):  
Carmen Dobjanschi ◽  
Rucsandra Dănciulescu Miulescu

AbstractWomen with gestational diabetes mellitus (GDM) have an increased lifetime risk of developing type 2 diabetes mellitus (T2DM). GDM has a substantial impact on maternal and foetal short and long-term health. Risk factors for GDM may be genetic or nongenetic and have been analysed in numerous studies. Researches in recent years allowed the identification of other risk factors for GDM except for those already known. Knowledge and identification of all risk factors for GDM allows the elaboration of a prevention strategy of T2DM, it may influence the screening, diagnosis, and, subsequently, treatment modalities for this disease.


2009 ◽  
Vol 296 (4) ◽  
pp. E936-E944 ◽  
Author(s):  
Michael J. Riedel ◽  
Corinna Wai Kwan Lee ◽  
Timothy J. Kieffer

Glucagon-like peptide (GLP)-1 is an incretin hormone with well-characterized antidiabetic properties, including glucose-dependent stimulation of insulin secretion and enhancement of β-cell mass. GLP-1 agonists have recently been developed and are now in clinical use for the treatment of type 2 diabetes. Rapid degradation of GLP-1 by enzymes including dipeptidyl-peptidase (DPP)-IV and neutral endopeptidase (NEP) 24.11, along with renal clearance, contribute to a short biological half-life, necessitating frequent injections to maintain therapeutic efficacy. Gene therapy may represent a promising alternative approach for achieving long-term increases in endogenous release of GLP-1. We have developed a novel strategy for glucose-regulated production of GLP-1 in hepatocytes by expressing a DPP-IV-resistant GLP-1 peptide in hepatocytes under control of the liver-type pyruvate kinase promoter. Adenoviral delivery of this construct to hepatocytes in vitro resulted in production and secretion of bioactive GLP-1 as measured by a luciferase-based bioassay developed to detect the NH2-terminally modified GLP-1 peptide engineered for this study. Transplantation of encapsulated hepatocytes into CD-1 mice resulted in an increase in plasma GLP-1 levels that was accompanied by a significant reduction in fasting plasma glucose levels. The results from this study demonstrate that a gene therapy approach designed to induce GLP-1 production in hepatocytes may represent a novel strategy for long-term secretion of bioactive GLP-1 for the treatment of type 2 diabetes.


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