Paul Pilch

ORCID iD
https://orcid.org/0000-0003-1997-0499
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BU Profiles

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Paul Pilch (2016-05-09)

Biochemistry Faculty

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Paul Pilch (2016-05-09)

Biochemistry Faculty

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Boston University (2018-04-17)

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0000-0003-1997-0499 (2013-09-23)

Biography

Research Interests: Cell biology of fuel utilization in adipocytes and skeletal muscle. The modern Western diet coupled with a sedentary lifestyle has led to an epidemic of obesity, a consequence of which is a dramatic rise in the incidence of type II diabetes mellitus, a malfunction in insulin-regulated metabolism. At the cellular level, type II diabetes is characterized by failure of insulin to act in liver, muscle and fat. We study aspects of insulin signaling and action in the latter two tissues. Insulin resistance in muscle (and fat) derives from the failure of insulin to activate the tissue-specific glucose transporter GLUT4. The activation mechanism for this process involves vesicle trafficking and protein targeting with regard to GLUT4 and the insulin receptor. We are characterizing the formation and protein content of GLUT4-containing vesicles; we are trying to identify the organelles through which they pass on their way to and from the cell surface and we are determining the communication mechanism(s) (signaling) from the insulin receptor to the GLUT4-containing vesicles. These studies involve both fat and muscle cells, and we are also studying the physiological role of cell surface (plasma membrane) micro-domains called caveolae that are particularly abundant in these tissues. We have evidence for the hypothesis that caveolae (for little caves that are small invaginations of the plasma membrane into the cytosol) are involved in lipid trafficking. We continue to study other aspects of adipocyte and muscle cell biology to understand the interplay between glucose and fat metabolism as well as the interplay between adipocytes and muscle required for overall metabolic homeostasis. Indeed, we wish to uncover the mechanism(s) by exercise also regulates some of these same parameters independent of insulin. Understanding these pathways will help us to figure out how they are compromised in pathophysiological states such as diabetes.

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