Sugar kills good cholesterol,

sugar

sugar

Scientists at the University of Warwick have discovered that ‘good’ cholesterol is turned ‘bad’ by a sugar-derived substance.

The substance, methylglyoxal – MG, was found to damage ‘good’ HDL cholesterol, which removes excess levels of bad cholesterol from the body.

Low levels of HDL, High Density Lipoprotein, are closely linked to heart disease, with increased levels of MG being common in the elderly and those with diabetes or kidney problems.

Supported by funding from the British Heart Foundation (BHF) and published in Nutrition and Diabetes, the researchers discovered that MG destabilises HDL and causes it to lose the properties which protect against heart disease.

HDL damaged by MG is rapidly cleared from the blood, reducing its HDL content, or remains in plasma having lost its beneficial function.

Lead researcher Dr Naila Rabbani, of the Warwick Medical School, says that: “MG damage to HDL is a new and likely important cause of low and dysfunctional HDL, and could count for up to a 10% risk of heart disease”.

There are currently no drugs that can reverse low levels of HDL, but the Warwick researchers argue that by discovering how MG damages HDL has provided new potential strategies for reducing MG levels.

Commenting on the research’s implications Dr Rabbani said:

“By understanding how MG damages HDL we can now focus on developing drugs that reduce the concentration of MG in the blood, but it not only be drugs that can help.

“We could now develop new food supplements that decrease MG by increasing the amount of a protein called glyoxalase 1, or Glo 1, which converts MG to harmless substances.

“This means that in future we have both new drugs and new foods that can help prevent and correct low HDL, all through the control of MG.”

A potentially damaging substance, MG is formed from glucose in the body. It is 40,000 times more reactive than glucose it damages arginine residue (amino acid) in HDL at functionally important site causing the particle to become unstable.

Glo1 converts MG to harmless substances and protects us. MG levels are normally kept low in the body to maintain good health but they slowly increase with ageing as Glo1 slowly becomes worn out and is only slowly replaced.

Dr Rabbani says: “We call abnormally high levels of MG ‘dicarbonyl stress’. This occurs in some diseases – particularly diabetes, kidney dialysis, heart disease and obesity. We need sufficient Glo1 to keep MG low and keep us in good health.”

Source:   eurekalert.org

Type 2 diabetes genes and metabolic markers

Type 2 diabetes: New associations identified between genes and metabolic markers:

diabetes-graphic

 

 

 

 

In two comprehensive studies, scientists from Helmholtz Zentrum Muenchen, Ludwig-Maximilians-Universitaet Muenchen and Technische Universitaet Muenchen discovered new associations of two major Type 2 diabetes risk genotypes and altered plasma concentrations of metabolic products. The “Virtual Institute Diabetes” joint research cooperation is thereby making an important contribution towards explaining the genetic and molecular basis of diabetes, The results have been published in the journals PLOS ONE and Metabolomics.

For these investigations, participants of the population-based cohort study KORA* carrying high-risk diabetes gene variants without having a diagnosed diabetes, as well as participants without an increased diabetes risk were recruited.

All study participants were subjected to a metabolic load. The nutritients, particularly sugars and fats, were administered either orally or intravenously. The scientists subsequently determined the concentrations of 163 metabolic products in blood samples from the participants. The teams headed by Prof. Dr. Thomas Illig (HMGU) and Dr. Harald Grallert (HMGU), Prof. Dr. Jochen Seißler (LMU), and Prof. Dr. Hans Hauner (TUM) and Dr. Helmut Laumen (TUM) were the first to supply a comprehensive characterisation of the metabolic performance in regard to the respective genotype.

It was observed that the concentrations of the recorded substances represent a particular metabolomic response pattern depending on the genotype. It was possible to verify specific metabolic effects, particularly for the TCF7L2 genotype, which is associated with an increased risk of type 2 diabetes. “We are aware of certain high-risk gene variants for type 2 diabetes. However, the causative mechanisms on the path to this disease are still largely unknown. With our results, we are helping to close the gap between disease-associated genes on the one hand and the development of diabetes on the other. A typically changed metabolic performance can supply early indications of diabetes”, explain Simone Wahl from HMGU and Cornelia Then from LMU, first authors of the two publications.

The scientists are currently investigating metabolic responses in additional genotypes. The objective is to advance the fundamental research on the widespread disease diabetes and to contribute the acquired knowledge to the clinical cooperation groups that have developed from the VID in order to promote the knowledge transfer between the laboratory and clinical care of patients suffering from diabetes.

American Deaths Surpass 2.5 Million

U.S. Mortality Rate: Deaths Surpass 2.5 Million For The First Time:

 U.S. Mortality Rate: Deaths Surpass 2.5 Million For The First Time


U.S. Mortality Rate: Deaths Surpass 2.5 Million For The First Time

U.S. deaths surpassed 2.5 million for the first time last year, reflecting the nation’s growing and aging population. The increase of about 45,000 more deaths than in 2010 was not surprising. The annual number of deaths has been generally rising for decades as the population has swelled. “If you have an older population, of course you have more deaths,” said Qian Cai, a University of Virginia demographer who studies population trends. “That doesn’t mean the population is less healthy or less vital.” Before last year, the largest number of deaths was 2.47 million in 2008. The number of deaths can jump up or down from year to year, depending on whether there was a bad flu season or other factors. The Centers for Disease Control and Prevention released the report Wednesday. It’s drawn from a review of most death certificates from last year. The report found that the rate of deaths per 100,000 people actually dropped to an all-time low. That was offset by the fact that there are so many Americans — about 314 million. Other report highlights:

—U.S. life expectancy for a child born in 2011 was about 78 years and 8 months, the same as it was in 2010.

—Women aren’t outliving men as much as they used to. The gap in life expectancy between the sexes, which was nearly 8 years at its widest in 1979, remained at less than 5 years in 2011.

—The infant mortality rate dropped again slightly, to a new low of 6.05 deaths per 1,000 births.

—Heart disease and cancer remain the top killers, accounting for nearly half the nation’s deaths. But the death rates from both continued to decline.

—Death rates fell for three other leading causes: stroke, Alzheimer’s disease and kidney disease.

Flu and pneumonia became the 8th leading killer, replacing kidney disease. Also increasing were the death rates for diabetes, chronic lower respiratory diseases, chronic liver disease and cirrhosis, Parkinson’s disease, and pneumonitis. The rise in pneumonitis deaths is another sign of an aging population. Mainly in people 75 and older, it happens when food or vomit goes down the windpipe and causes deadly damage to the lungs. The increase in deaths is occurring at a time U.S. births have been falling for several years, but there more than enough newborns to replace Americans who die. The number of births last year was close to 4 million. Add in immigrants, and the total population is growing by 2 million to 3 million people a year.

 

Diabetes Associated With Iron Transport

 

Diabetes Cause may be Associated With Iron Transport:

Diabetes Cause may be Associated With Iron Transport

Diabetes Cause may be Associated With Iron Transport

Increased activity of a iron-transport protein destroys insulin-producing beta cells and thereby contributes to diabetes. In addition, the new research shows that mice without this iron transporter are protected against developing diabetes. These results have just been published in the prestigious journal Cell Metabolism. Almost 300,000 Danes have diabetes – 80 per cent have type-2 diabetes, a so-called lifestyle disease. The number of people with diabetes doubles every decade and the disease costs Danish society about DKK 86 million per day. People develop diabetes when the beta cells in their pancreas do not produce enough insulin to meet their body’s needs. New research from the University of Copenhagen and Novo Nordisk A/S links this defect to one particular cellular iron transporter. “Iron is a vital mineral for the healthy functioning of the body and is found in many enzymes and proteins, for example, the red blood pigment that transports oxygen. But iron can also promote the creation of toxic oxygen radicals. An increase in the iron content of the cells may cause tissue damage and disease. We find that increased activity of a certain iron transporter causes damage to the beta cell. And if we completely remove this iron transporter in the beta cells in genetically engineered mice, they are indeed protected against diabetes,” explains Professor Thomas Mandrup-Poulsen, Department of Biomedical Sciences, The Faculty of Health and Medical Sciences. Together with Christina Ellervik, Associate Professor and Professors Børge Nordestgaard and Henrik Birgens from the University of Copenhagen, Thomas Mandrup-Poulsen has previously documented a connection between surplus iron and diabetes risk, based on large population studies. But this is the first time that scientists have found a link between inflammation and iron transport, which appears to be the underlying cause of the observed higher risk. “We need to conduct controlled clinical trials showing that changes in the iron content of the body can reduce the risk of diabetes. Only then will we be able to advise people at risk of diabetes not to take iron supplements, or recommend drug treatment to reduce the amount of iron in the body,” says Thomas Mandrup-Poulsen. The team behind the scientific article in Cell Metabolism can see that the inflammatory signal substances created around the beta cells in both type-1 and type-2 diabetes accelerate the activity of the iron transporter. “The evolutionary explanation of why the highly specialised beta cells are influenced by the inflammatory signal substances and contain the potentially dangerous iron transport proteins is presumably that the short-term increase in the amount of oxygen radicals is critical to the fine-tuning of insulin production during bouts of fever and stress. However, nature had not foreseen the long-term local production of signal substances around the beta cells, which we see in type-1 and type-2 diabetes,” continues Thomas Mandrup-Poulsen. The new results have implications for many scientists, not only those conducting research in diabetes. The beta cell can be used as a model for other cells that are particularly sensitive to iron, such as liver cells and cardiac-muscle cells.

 

Alzheimer’s as Type 3 diabetes

Alzheimer’s could be reclassified as Type 3 diabetes:
Alzheimer's could be reclassified as Type 3 diabetes

Alzheimer’s could be reclassified as Type 3 diabetes

Growing evidence that Alzheimer’s is primarily a metabolic disease has led some researchers to propose reclassifying it as Type 3 diabetes, according to the Guardian. Such a revelation could have profound implications on the role that the junk food industry plays in causing Alzheimer’s. Today an estimated 35 million people suffer from Alzheimer’s disease around the world, and as many as 346 million people suffer from diabetes. Both numbers are expected to rise exponentially over the next several decades — rises that also happen to be correlated with increasing obesity rates. The correlation is so uncanny that many scientists are investigating a causal relationship between all three epidemics, with staggering results. Type 2 diabetes has already been strongly linked with obesity and diet as well as with dementia and Alzheimer’s. For instance, Type 2 sufferers are two to three times more likely to get Alzheimer’s than the general population. The link between Alzheimer’s and obesity has been studied less, but a growing cacophony of research is filling that gap. For instance, studies have strongly linked midlife obesity to Alzheimer’s. Fitness and a better diet have also been linked to a decreased occurrence of dementia. Now new studies are suggesting a link even more profound: that Alzheimer’s may be caused directly by the brain’s impaired response to insulin. A 2005 report found that levels of both insulin and insulin-like growth factors in the brains of Alzheimer’s patients were lower than normal, with the lowest levels being found in the brain regions most devastated by the disease. Meanwhile, a report released just last year found that an insulin spray helped improve memory skills in people with Alzheimer’s. Insulin has a well-defined role in the brain’s chemistry. It helps regulate the transmission of signals between neurons. It’s not difficult to begin connecting the dots at this point. A causal relationship between Alzheimer’s and the brain’s insulin regulation isn’t difficult to imagine and detail. Of course, more research needs to be done to know for sure, but if Alzheimer’s and other kinds of dementia are proven to be another form of diabetes, then the obesity epidemic — and the junk food industry that fuels it — could have consequences on public health that are even more profound than previously realized.