Mary-Elizabeth Patti, M.D.
|Title||Assistant Professor of Medicine|
|Institution||Joslin Diabetes Center|
|Address||Joslin Diabetes Center|
Cellular & Mol. Physiology
One Joslin Place
Boston MA 02215
Available: 09/01/13, Expires: 08/31/14
Obesity and type 2 diabetes (T2D) are major public health challenges for our generation. Particularly concerning is the rise in obesity in the pediatric population, the anticipated rise in premature morbidity and mortality with long-standing obesity and costs associated with obesity-related. In parallel, recent projections suggest that prevalence of diabetes is likely to increase to over 25% of the US population by 2050, yielding enormous tolls at individual, public health, and economic levels. Unfortunately, there are no simple answers for the dual epidemics of obesity and T2D. Novel insights and approaches on many fronts are required.
Risk patterns for both obesity and T2D can originate as a consequence of alterations in growth and metabolism during critical windows of prenatal and early postnatal development. Moreover, obesity, prediabetes, and diabetes in individuals of reproductive age can initiate a vicious cycle, propagating risk to subsequent generations via non-genetic, or epi-genetic and metabolic mechanisms. Thus, understanding mechanisms mediating these effects is an important scientific and clinical goal. More importantly, this concept provides the hope that identification of high-risk individuals for targeted intervention during early childhood and subsequent reproductive life may limit vicious cycles of metabolic risk.
One example of nutritionally-mediated transmission of metabolic phenotypes is provided from our laboratory’s mouse model in which healthy pregnant mothers (F0) are exposed to modified nutrition during the last third of pregnancy. Their offspring (F1) have a modest 15% reduction in birth weight and experience early postnatal “catch-up growth.” Despite normal chow diet after weaning, these UN-exposed mice go on to develop progressive glucose intolerance, insulin secretory dysfunction, reduced muscle mass, and obesity as adults. UN exposed mice have upregulation of lipogenic gene expression in both liver and adipose, increased adipocyte size, and reduced mitochondrial DNA content. We have recently demonstrated that UN-exposed mice also have reduced numbers of myogenic precursor cells, suggesting the possibility that alterations in key stem cell populations may alter developmental trajectories and modify tissue structure/function and repair. The goal of the current study is to examine patterns of transcriptional dysregulation in myoblasts isolated from skeletal muscle from at-risk mice, and in parallel, to identify potential epigenetic mediators resulting from exposure to nutritional stress during pregnancy.
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