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Mice studies very often do not follow through for humans but could this be the start of why some people who were never over weight all their adult lives, suddenly become over weight, and then further down the line become type diabetics.
"Researchers with the UT Southwestern's Touchstone Center for Diabetes found that giving mice high levels of insulin, which is typically done to counter the effects of diabetes or insulin resistance in Type 2 diabetes, also fosters processes that lead to obesity.
"The discovery was made by studying mice engineered to lack receptors for a hormone called glucagon.
Glucagon spurs the liver's production of glucose into the bloodstream and thus maintains the fuel supply for the brain. Insulin blocks the secretion of glucagon, opposes glucagon action on the liver, and instructs the body to take up glucose from the blood. Type 2 diabetics cannot respond properly to insulin and have uncontrolled glucagon production, thereby causing their livers to overproduce glucose, contributing to high blood-sugar levels. Insulin is often given to people with type 2 diabetes to try to overcome insulin-resistance and lower the levels of glucose in the bloodstream.
But insulin also signals the body to produce fat, so when given the high levels of insulin needed to control excess glucose, mice become fat, explained corresponding author Dr. Michael Roth, Professor of Biochemistry at UT Southwestern and a member of the Touchstone Diabetes Center.
"We found that mice lacking the receptor for glucagon cannot get fat unless they are given the high levels of insulin found in mice (and humans) that have type 2 diabetes," said Dr. Roth, who holds the Diane and Hal Brierley Distinguished Chair in Biomedical Research. "This result suggests that the high levels of insulin found in those who develop insulin resistance and type 2 diabetes are a contributor to obesity and its complications."
More on this story here http://www.sciencedaily.com/releases/2014/08/140825185319.htm
Regards Eddie
"Researchers with the UT Southwestern's Touchstone Center for Diabetes found that giving mice high levels of insulin, which is typically done to counter the effects of diabetes or insulin resistance in Type 2 diabetes, also fosters processes that lead to obesity.
"The discovery was made by studying mice engineered to lack receptors for a hormone called glucagon.
Glucagon spurs the liver's production of glucose into the bloodstream and thus maintains the fuel supply for the brain. Insulin blocks the secretion of glucagon, opposes glucagon action on the liver, and instructs the body to take up glucose from the blood. Type 2 diabetics cannot respond properly to insulin and have uncontrolled glucagon production, thereby causing their livers to overproduce glucose, contributing to high blood-sugar levels. Insulin is often given to people with type 2 diabetes to try to overcome insulin-resistance and lower the levels of glucose in the bloodstream.
But insulin also signals the body to produce fat, so when given the high levels of insulin needed to control excess glucose, mice become fat, explained corresponding author Dr. Michael Roth, Professor of Biochemistry at UT Southwestern and a member of the Touchstone Diabetes Center.
"We found that mice lacking the receptor for glucagon cannot get fat unless they are given the high levels of insulin found in mice (and humans) that have type 2 diabetes," said Dr. Roth, who holds the Diane and Hal Brierley Distinguished Chair in Biomedical Research. "This result suggests that the high levels of insulin found in those who develop insulin resistance and type 2 diabetes are a contributor to obesity and its complications."
More on this story here http://www.sciencedaily.com/releases/2014/08/140825185319.htm
Regards Eddie
