Community based early intervention for the prevention of type 2 diabetes: A case report of the Kahnawake schools diabetes prevention project
- Authors: Nield, Alex , Quarrell, Sean , Myers, Stephen
- Date: 2013
- Type: Text , Journal article
- Relation: Journal of Diabetes and Metabolism Vol. 4, no. 6 (2013), p. 1-6
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- Description: Type 2 diabetes (T2D) is a chronic metabolic disorder that is predominately associated with lifestyle changes including reduced physical activity, poor nutrition and obesity. Despite major medical advances in the treatment of T2D, its prevalence is still increasing at an alarming rate. Accordingly, better management and prevention strategies are urgently needed to prevent the development and progression of this disease. In the last decade there have been considerable efforts to improve public health through alternative research paradigms. Community-Based Participatory Research (CBPR) is one such process by which researchers form an equal and transparent partnership with the community with the final goal of creating empowerment and societal change to facilitate action and provide solutions to promote health and well-being. One CBPR program, the Kahnawake Schools Diabetes Prevention Project (KSDPP), was initiated to promote increased physical activity and healthier eating habits among school children based on the Mohawk’s “Living in Balance” philosophy. Utilizing CBPR principles, KSDPP engaged researchers and the community in all stages of the research processes. This project was community driven from the beginning and was independent of any external institutional change agent to facilitate community action and the implementation of strategies to find solutions. Although the project has been instrumental in community empowerment and societal change, several challenges remain. Accordingly, understanding the unique social, environmental and historical context that shapes lifestyle and risk factors for T2D in Native populations will help to understand the unique nature of this disease in these groups.
The Zinc Transporter, Slc39a7 (Zip7) Is Implicated in Glycaemic Control in Skeletal Muscle Cells
- Authors: Myers, Stephen , Nield, Alex , Chew, Guatsiew , Myers, Mark
- Date: 2013
- Type: Text , Journal article
- Relation: Plos One Vol. 8, no. 11 (November 2013 2013), p. 15
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- Description: Dysfunctional zinc signaling is implicated in disease processes including cardiovascular disease, Alzheimer's disease and diabetes. Of the twenty-four mammalian zinc transporters, ZIP7 has been identified as an important mediator of the 'zinc wave' and in cellular signaling. Utilizing siRNA targeting Zip7 mRNA we have identified that Zip7 regulates glucose metabolism in skeletal muscle cells. An siRNA targeting Zip7 mRNA down regulated Zip7 mRNA 4.6-fold (p = 0.0006) when compared to a scramble control. This was concomitant with a reduction in the expression of genes involved in glucose metabolism including Agl, Dlst, Galm, Gbe1, Idh3g, Pck2, Pgam2, Pgm2, Phkb, Pygm, Tpi1, Gusb and Glut4. Glut4 protein expression was also reduced and insulin-stimulated glycogen synthesis was decreased. This was associated with a reduction in the mRNA expression of Insr, Irs1 and Irs2, and the phosphorylation of Akt. These studies provide a novel role for Zip7 in glucose metabolism in skeletal muscle and highlight the importance of this transporter in contributing to glycaemic control in this tissue.
Zinc transporters, mechanisms of action and therapeutic utility : Implications for type 2 diabetes mellitus
- Authors: Myers, Stephen , Nield, Alex , Myers, Mark
- Date: 2012
- Type: Text , Journal article
- Relation: Journal of Nutrition and Metabolism Vol. 2012, no. (2012), p. 1-13
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- Description: Zinc is an essential trace element that plays a vital role in maintaining many biological processes and cellular homeostasis. Dysfunctional zinc signaling is associated with a number of chronic disease states including cancer, cardiovascular disease, Alzheimer's disease, and diabetes. Cellular homeostasis requires mechanisms that tightly control the uptake, storage, and distribution of zinc. This is achieved through the coordinated actions of zinc transporters and metallothioneins. Evidence on the role of these proteins in type 2 diabetes mellitus (T2DM) is now emerging. Zinc plays a key role in the synthesis, secretion and action of insulin in both physiological and pathophysiological states. Moreover, recent studies highlight zinc's dynamic role as a "cellular second messenger" in the control of insulin signaling and glucose homeostasis. This suggests that zinc plays an unidentified role as a novel second messenger that augments insulin activity. This previously unexplored concept would raise a whole new area of research into the pathophysiology of insulin resistance and introduce a new class of drug target with utility for diabetes pharmacotherapy. © 2012 Stephen A. Myers et al.
- Description: 2003010692
Zinc, zinc transporters and Type 2 Diabetes
- Authors: Myers, Stephen , Nield, Alex
- Date: 2014
- Type: Text , Book chapter
- Relation: Endocrine diseases Chapter 2 p.
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- Description: Insulin resistance is an important characteristic of Type 2 Diabetes (T2D) and is commonly associated with obesity, hypertension and cardiovascular disease (Carsten, 2000; Hulver and Lynis, 2004). Insulin resistance reduces insulin-stimulated glucose disposal due to multiple post-recepter intracellular defects in insulin signaling with subsequent reductions in glucose transport, glucose oxidation and incorporation of glucose into glycogen (Abdul-Ghani and DeFronzo, 2010; Peppa et al., 2010). The intracellular post-receptor regulatory effects of insulin include the regulation of the cellular glucose transport system, adaptive changes in gene expression and subsequent biosynthesis and action of the enzymes involved in the preservation of metabolism, and the modulation of genes that contribute to increased pro-mitotic, proliferative and anti-apoptotic activity of cells (Taton et al., 2010). Accordingly, the reduced activity of insulin action in any, or all of these post-receptor regulatory actions is insulin resistance. Given that insulin resistance usually precedes the development of T2D and is a major component of the progressive nature of this disease (Pagel-Langenickel et al., 2010), understanding the pathophysiology of insulin resistance will enable the development of therapeutic strategies to prevent or manage disease progression. Although many theories have been forthcoming, the primary mechanism of insulin resistance remains largely elusive.