Role in Diabetes
Excess Fructose May Play Role in Diabetes, Obesity and Other Health Conditions
More and more people have become aware of the dangers of excessive fructose in diet. A new review on fructose in an upcoming issue of the Journal of the American Society of Nephrology (JASN) indicates just how dangerous this simple sugar may be.Richard J. Johnson, MD and Takahiko Nakagawa, MD (Division of Renal Diseases and Hypertension, University of Colorado) provide a concise overview of recent clinical and experimental studies to understand how excessive amounts of fructose, present in added sugars, may play a role in high blood pressure, diabetes, obesity, and chronic kidney disease (CKD).
Dietary fructose is present primarily in added dietary sugars, honey, and fruit. Americans most frequently ingest fructose from sucrose, a disaccharide containing 50% fructose and 50% glucose bonded together, and high fructose corn syrup (HFCS), a mixture of free fructose and free glucose, usually in a 55/45 proportion. With the introduction of HFCS in the 1970s, an increased intake of fructose has occurred and obesity rates have risen simultaneously.
The link between excessive intake of fructose and metabolic syndrome is becoming increasingly established. However, in this review of the literature, the authors conclude that there is also increasing evidence that fructose may play a role in hypertension and renal disease. "Science shows us there is a potentially negative impact of excessive amounts of sugar and high fructose corn syrup on cardiovascular and kidney health," explains Dr. Johnson. He continues that "excessive fructose intake could be viewed as an increasingly risky food and beverage additive."
Concerned that physicians may be overlooking this health problem when advising CKD patients to follow a low protein diet, Dr. Johnson and Dr. Nakagawa recommend that low protein diets include an attempt to restrict added sugars containing fructose.
Dr. Johnson and Dr. Nakagawa are listed as inventors on several patent applications related to lowering uric acid for the treatment or prevention of hypertension, diabetes, and fatty liver.
Obesity and Diabetes: Immune Cells in Fat Tissue Explain the Link
Inflammation-causing cells in fat tissue may explain the link between obesity and diabetes, a team of Walter and Eliza Hall Institute researchers in Melbourne, Australia, has shown.The discovery, by Professor Len Harrison and Dr John Wentworth from the institute's Autoimmunity and Transplantation division, opens the way for new anti-inflammatory treatments that prevent insulin resistance (where the body is unable to respond to and use the insulin it produces) and other complications associated with obesity.
"We have shown that insulin resistance in human obesity is closely related to the presence of inflammatory cells in fat tissue, in particular a population of macrophage cells," Professor Harrison said.
Macrophages, white blood cells derived from the bone marrow, are immune cells that normally respond to infections. In obese people, macrophages move into the fat tissue where they cause inflammation and release cytokines, which are chemical messenger molecules used by immune cells to communicate. Certain cytokines cause cells to become resistant to the effects of the hormone insulin, leading to diabetes and heart disease.
Professor Harrison and Dr Wentworth worked with Mr Gaetano Naselli, Ms Belinda Phipson and Dr Gordon Smyth at the institute as well as Professor Paul O'Brien at Monash University's Centre for Obesity Research and Education to analyse the fat tissue of more than 100 Victorians who had undergone lapband surgery.
Their findings, published in the journal Diabetes, provide the first evidence in humans that macrophages in the fat tissue are producing cytokines that prevent cells from appropriately responding to the presence of insulin.
"The complications of obesity such as insulin resistance and diabetes, cardiovascular disease associated with hardening of the arteries, and liver problems are the result of inflammation that occurs in the fat tissue," Professor Harrison said. "These complications could be prevented by developing drugs that target certain cytokines released by the macrophages.
"Encouragingly, our study also showed that when obese people lost weight the macrophages in the fat tissue disappeared, as did the risk of developing insulin resistance and diabetes."
Diabetes affects more than a million Australians and is a disease in which the body does not produce or properly use insulin, a hormone necessary to convert sugar, starches and other food into the energy needed for daily life.
The research was supported by the Australian National Health and Medical Research Council, the Victorian Government, Diabetes Australia Research Trust and the Royal Australasian College of Physicians Research Foundation.
More and more people have become aware of the dangers of excessive fructose in diet. A new review on fructose in an upcoming issue of the Journal of the American Society of Nephrology (JASN) indicates just how dangerous this simple sugar may be.Richard J. Johnson, MD and Takahiko Nakagawa, MD (Division of Renal Diseases and Hypertension, University of Colorado) provide a concise overview of recent clinical and experimental studies to understand how excessive amounts of fructose, present in added sugars, may play a role in high blood pressure, diabetes, obesity, and chronic kidney disease (CKD).
Dietary fructose is present primarily in added dietary sugars, honey, and fruit. Americans most frequently ingest fructose from sucrose, a disaccharide containing 50% fructose and 50% glucose bonded together, and high fructose corn syrup (HFCS), a mixture of free fructose and free glucose, usually in a 55/45 proportion. With the introduction of HFCS in the 1970s, an increased intake of fructose has occurred and obesity rates have risen simultaneously.
The link between excessive intake of fructose and metabolic syndrome is becoming increasingly established. However, in this review of the literature, the authors conclude that there is also increasing evidence that fructose may play a role in hypertension and renal disease. "Science shows us there is a potentially negative impact of excessive amounts of sugar and high fructose corn syrup on cardiovascular and kidney health," explains Dr. Johnson. He continues that "excessive fructose intake could be viewed as an increasingly risky food and beverage additive."
Concerned that physicians may be overlooking this health problem when advising CKD patients to follow a low protein diet, Dr. Johnson and Dr. Nakagawa recommend that low protein diets include an attempt to restrict added sugars containing fructose.
Dr. Johnson and Dr. Nakagawa are listed as inventors on several patent applications related to lowering uric acid for the treatment or prevention of hypertension, diabetes, and fatty liver.
Obesity and Diabetes: Immune Cells in Fat Tissue Explain the Link
Inflammation-causing cells in fat tissue may explain the link between obesity and diabetes, a team of Walter and Eliza Hall Institute researchers in Melbourne, Australia, has shown.The discovery, by Professor Len Harrison and Dr John Wentworth from the institute's Autoimmunity and Transplantation division, opens the way for new anti-inflammatory treatments that prevent insulin resistance (where the body is unable to respond to and use the insulin it produces) and other complications associated with obesity.
"We have shown that insulin resistance in human obesity is closely related to the presence of inflammatory cells in fat tissue, in particular a population of macrophage cells," Professor Harrison said.
Macrophages, white blood cells derived from the bone marrow, are immune cells that normally respond to infections. In obese people, macrophages move into the fat tissue where they cause inflammation and release cytokines, which are chemical messenger molecules used by immune cells to communicate. Certain cytokines cause cells to become resistant to the effects of the hormone insulin, leading to diabetes and heart disease.
Professor Harrison and Dr Wentworth worked with Mr Gaetano Naselli, Ms Belinda Phipson and Dr Gordon Smyth at the institute as well as Professor Paul O'Brien at Monash University's Centre for Obesity Research and Education to analyse the fat tissue of more than 100 Victorians who had undergone lapband surgery.
Their findings, published in the journal Diabetes, provide the first evidence in humans that macrophages in the fat tissue are producing cytokines that prevent cells from appropriately responding to the presence of insulin.
"The complications of obesity such as insulin resistance and diabetes, cardiovascular disease associated with hardening of the arteries, and liver problems are the result of inflammation that occurs in the fat tissue," Professor Harrison said. "These complications could be prevented by developing drugs that target certain cytokines released by the macrophages.
"Encouragingly, our study also showed that when obese people lost weight the macrophages in the fat tissue disappeared, as did the risk of developing insulin resistance and diabetes."
Diabetes affects more than a million Australians and is a disease in which the body does not produce or properly use insulin, a hormone necessary to convert sugar, starches and other food into the energy needed for daily life.
The research was supported by the Australian National Health and Medical Research Council, the Victorian Government, Diabetes Australia Research Trust and the Royal Australasian College of Physicians Research Foundation.
