tamarian
Tue, Jun-19-01, 23:43
Monday June 18
New Protein Linked to Type 2 Diabetes
By Will Boggs, MD
NEW YORK (Reuters Health) - Abnormal production of a recently discovered protein called UCP2 (for uncoupling protein-2) may account for type 2 diabetes, the form seen most commonly in obese individuals.
UCP2 is produced by a variety of tissues, including the beta-cells of the pancreas that produce insulin, the hormone responsible for controlling glucose (sugar) levels in the body, according to Dr. Bradford B. Lowell, from Harvard Medical School (news - web sites), in Boston, and associates.
Because previous studies indicated a possible role for UCP2 in regulating insulin secretion, the authors studied its function in greater detail by examining mice bred to produce low levels of UCP2 or to produce none at all.
According to the report in the June 15th issue of Cell, mice lacking in UCP2 had higher insulin levels and lower blood glucose levels than did normal mice. These mice also secreted greater amounts of insulin in response to a sugary meal than normal mice did. The researchers also found that pancreas cells from a strain of obese mice that develop type 2 diabetes produce higher levels of UCP2 than do other mice, suggesting that overproduction of UCP2 could promote the development of diabetes.
The scientists then crossbred the obese mice with the UCP2-deficient mice. The resulting mice were still obese, they say, but the lack of UCP2 resulted in a marked improvement in their blood sugar levels. The researchers attribute this improvement to improved beta-cell function in the face of lower UCP2 levels.
``These findings raise the possibility that inhibitors of UCP2 activity, by increasing insulin secretion, could offer a novel means of treating type 2 diabetes,'' the authors conclude.
``To my knowledge there have been no published studies which have specificallyexamined the link between polymorphisms minor mutations in UCP2 gene sequence and type 2 diabetes in humans,'' Lowell told Reuters Health via e-mail.
``Using genetic engineering approaches in mice, we have generated strong support for the hypothesis that induction of UCP2 is a link between obesity and pancreatic beta-cell dysfunction,'' he continued. Further research will be needed to determine whether this mechanism is at work in all mouse models of type 2 diabetes and, more importantly, in human type 2 diabetes, he added.
``The suggestion that pancreatic beta-cell UCP2 is a useful target for the therapy of type 2 diabetes is exciting,'' agree Dr. Kenneth S. Polonsky and Dr. Clay F. Semenkovich, from Washington University School of Medicine, in St. Louis, Missouri, in a related commentary
http://dailynews.yahoo.com/h/nm/20010618/hl/diabetes_9.html
New Protein Linked to Type 2 Diabetes
By Will Boggs, MD
NEW YORK (Reuters Health) - Abnormal production of a recently discovered protein called UCP2 (for uncoupling protein-2) may account for type 2 diabetes, the form seen most commonly in obese individuals.
UCP2 is produced by a variety of tissues, including the beta-cells of the pancreas that produce insulin, the hormone responsible for controlling glucose (sugar) levels in the body, according to Dr. Bradford B. Lowell, from Harvard Medical School (news - web sites), in Boston, and associates.
Because previous studies indicated a possible role for UCP2 in regulating insulin secretion, the authors studied its function in greater detail by examining mice bred to produce low levels of UCP2 or to produce none at all.
According to the report in the June 15th issue of Cell, mice lacking in UCP2 had higher insulin levels and lower blood glucose levels than did normal mice. These mice also secreted greater amounts of insulin in response to a sugary meal than normal mice did. The researchers also found that pancreas cells from a strain of obese mice that develop type 2 diabetes produce higher levels of UCP2 than do other mice, suggesting that overproduction of UCP2 could promote the development of diabetes.
The scientists then crossbred the obese mice with the UCP2-deficient mice. The resulting mice were still obese, they say, but the lack of UCP2 resulted in a marked improvement in their blood sugar levels. The researchers attribute this improvement to improved beta-cell function in the face of lower UCP2 levels.
``These findings raise the possibility that inhibitors of UCP2 activity, by increasing insulin secretion, could offer a novel means of treating type 2 diabetes,'' the authors conclude.
``To my knowledge there have been no published studies which have specificallyexamined the link between polymorphisms minor mutations in UCP2 gene sequence and type 2 diabetes in humans,'' Lowell told Reuters Health via e-mail.
``Using genetic engineering approaches in mice, we have generated strong support for the hypothesis that induction of UCP2 is a link between obesity and pancreatic beta-cell dysfunction,'' he continued. Further research will be needed to determine whether this mechanism is at work in all mouse models of type 2 diabetes and, more importantly, in human type 2 diabetes, he added.
``The suggestion that pancreatic beta-cell UCP2 is a useful target for the therapy of type 2 diabetes is exciting,'' agree Dr. Kenneth S. Polonsky and Dr. Clay F. Semenkovich, from Washington University School of Medicine, in St. Louis, Missouri, in a related commentary
http://dailynews.yahoo.com/h/nm/20010618/hl/diabetes_9.html