Mary-Elizabeth Patti, M.D.
Associate Professor of Medicine
Joslin Diabetes Center
Joslin Diabetes Center
Cellular & Mol. Physiology
One Joslin Place
Boston MA 02215
Available: 09/03/19, Expires: 09/30/21
Obesity and type 2 diabetes (T2D) are major public health challenges for our generation. Unfortunately, there are no simple answers for the dual epidemics of obesity and T2D. Novel insights and approaches on many fronts are required. One new approach to target disease risk arises from the recognition that 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.
Our laboratory is studying mechanisms by which altered nutrition and metabolism can impact offspring, and to identify methods to reverse the impact of adverse exposures on offspring. Using our mouse model, we have demonstrated that mice exposed to transient nutritional alterations during their development go on to develop progressive glucose intolerance, insulin secretory dysfunction, reduced muscle mass, and obesity as adults – the classic phenotype of diabetes risk. Moreover, these F1 mice (both males and females) yield F2 offspring with abnormal glucose tolerance and increased adiposity. These data suggest that environmental exposures alter germ cell epigenetic marks, which may contribute to altered development in F2 offspring and increase risk of chronic disease. We are now testing (in both mice and humans!) whether interventions such as diet, activity, and medications which target specific pathways may reduce transmission of disease risk from one generation to the next.
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