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Mitchell A. Lazar, M.D., Ph.D.
answers a few questions about this month's fast breaking paper
in field of Multidisicplinary.
From
•>>February 2002
Field: Multidisciplinary
Article Title: "The hormone resistin links obesity to
diabetes."
Authors: Steppan,
CM;Bailey, ST;Bhat, S;Brown, EJ;Banerjee, RR;Wright, CM;Patel,
HR;Ahima, RS;Lazar,
MA
Journal: NATURE
Volume: 409
Page: 307-312
Year: JAN 18 2001
* Univ Penn, Sch Med, Dept Med, Div Endocrinol Diabet &
Metab, Philadelphia, PA 19104 USA.
* Univ Penn, Sch Med, Dept Med, Div Endocrinol Diabet &
Metab, Philadelphia, PA 19104 USA.
* Univ Penn, Sch Med, Dept Genet, Div Endocrinol Diabet &
Metab, Philadelphia, PA 19104 USA.
* Univ Penn, Sch Med, Penn Diabet Ctr, Philadelphia, PA 19104
USA.
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Why do you think your paper is highly cited?
This paper is highly cited because it represented a discovery of a newly
described molecule secreted by fat cells and regulated by
antidiabeticdrugs. Thus it has relevance to obesity and diabetes, two foci of tremendous
interest to biomedical researchers and the public because of the impact of
these diseases on our society. Much more work needs to be done, but the fact
that this opens up a new area of investigation probably accounts for the
high citation rate.
Does it describe a new discovery or new methodology that's useful to others?
This was a new discovery.
Could you summarize the significance of your paper in layman's terms?
There is little question that obesity predisposes to type 2 diabetes, but
the underlying explanation is not certain. The excess of fat cells somehow
makes the whole body resistant to the action of insulin. Fat cells have
recently been realized to be like endocrine organs, in that they produce
substances that act at a distance to regulate metabolism. These include
fatty acids, as well as proteins such as the hormone leptin that regulates
feeding and metabolism. Our paper described a novel mouse protein
secreted into the bloodstream only from fat cells. We called it
"resistin" because our evidence was consistent with its being one of the fat cell factors
related to resistance to insulin. If it proves to be a major contributor
to insulin resistance in human as well as mouse, then it might be a target
for future therapies for type 2 diabetes. Much more work needs to be done.
Mitchell A. Lazar, M.D., Ph.D.
Chief, Division of Endocrinology, Diabetes, and Metabolism
Director, Penn Diabetes Center
University of Pennsylvania School of Medicine
611 CRB
415 Curie Blvd.
Philadelphia, PA 19104
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ESI Special
Topics, February 2002
Citing URL - http://www.esi-topics.com/fbp/comments/february02-MitchellLazar.html
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