No, no elephants here. Sorry. This is about human trunks - that is, your upper torso. "Upper trunk fat" refers to fatty deposits that form on the chest and upper back area. According to the latest research, upper trunk fat is associated with increased risk for insulin resistance. And insulin resistance, in case ya didn't know, is an early symptom of type 2 diabetes.

It was already known that visceral fat, the fatty deposits that form around and between the internal organs, contributes to insulin resistance.

This study, linking upper trunk fat to insulin resistance, was conducted by researchers based at the San Francisco VA Medical Center. The connection was actually established in the course of a study of fat redistribution and metabolic change in HIV-infected patients. Both HIV-positive patients on antiretroviral therapy and non-HIV-infected control participants were involved in the study.

A surprise finding was this fact that upper trunk fat contributes to insulin resistance just as much as does visceral fat. Also of note: this occurs regardless of whether or not the other type of fat is present. The researchers also note that all study participants were equally at risk. Says lead researcher Dr. Carl Grunfeld, "Strikingly, there was very little difference between HIV-infected people and controls. If you have fat up top, it's bad for you."

A full report has been published in the online version of the Journal of Acquired Immune Deficiency Syndromes.

Did you hear about renowned Harvard scientist Barbara Kahn's latest published research? I blogged about it recently. Kahn and colleagues state, in a report published in Cell Metabolism (July 2007), that it's possible to use a simple blood test to detect the presence of a specific protein called RBP4. Kahn et al say the presence of RBP4 can be used to measure accumulations of deep belly fat. Underpinning this research is a belief that such accumulations of belly fat increase risk for metabolic syndrome, leading to various maladies including heart disease and diabetes.

However, not everyone accepts this point of view. A Yale research team says that deep belly fat may not be so evil after all. The researchers, who are based at Yale University School of Medicine in Chevy Chase, Maryland, assert that metabolic syndrome is caused not by belly fat but by insulin resistance in skeletal muscle. This resistance, they state, makes it tough for the body to manufacture glycogen, so - in people who are insulin resistant - energy that cannot be stored as glycogen gets diverted into fatty acid production, which then contributes to metabolic syndrome.

The team compared abdominal fat levels in young and healthy individuals, some of whom were insulin sensitive and some of whom were insulin resistant. The result? "There is absolutely no difference in the volume of abdominal fat," states Yale's Gerald I. Shulman, who was lead author of the study. Abdominal fat, says Dr. Shulman, "may come later in the course of the disease [metabolic syndrome], but it's not a primary, underlying factor."

The beta-blocker carvedilol does not cause weight gain in diabetic patients, declares a new study just out. Significance? It means the drug does away with a problematic side-effect of other (earlier) beta-blockers, which are medications prescribed to correct high blood pressure. The study has been published in the American Journal of Medicine (July 2007) and was conducted by researchers at St. Luke's-Roosevelt Hospital Center in New York.

Around eleven hundred patients participated in the study, all of whom have Type 2 diabetes and also suffer from high blood pressure. Some took the new drug carvedilol, while others were given the standard metoprolol. Over the course of five months the patients on metoprolol gained an average of 1.19 kg/2.6 lbs, whereas those on taking carvedilol experienced an average gain of 0.17 kg/0.37 lbs, which is considered insignificant.

Weight gain is an undesirable side-effect of medications in virtually any circumstance. However, it is particularly true for people with Type 2 diabetes or those at risk for T2 because overweight and obesity contributes to insulin resistance. In other words, weight gain will likely increase your chances of developing T2 if you're already predisposed or it will make your T2 worse if you already have it...putting you more at risk for the kinds of heart problems that beta-blockers are prescribed to treat! So it's no surprise that Franz H. Messerli, the lead author of the study, told Reuters that doctors should "avoid traditional beta-blockers such as atenolol and metoprolol in the diabetic hypertensive patient or in the hypertensive patient at risk for diabetes."

It used to be that fat was just fat. Not anymore. Turns out that even fat is, upon close examination, more complicated than we ever realized. Did you know, for instance, that accumulations of deep belly fat are particularly harmful? Such accumulations are a risk factor for Type 2 diabetes because they are associated with increased insulin resistance, not to mention increased risk of heart attack.

One problem with deep belly fat, however, is that you can't necessarily detect it with a tape measure or by eyeballing someone's waistline. That is, you can't tell by just looking at a person how much of the fat surrounding their abdomen is deep belly fat versus the subcutaneous fat that lies just under the skin's surface. However, a new study reports that a simple blood test could solve this problem by measuring quantities of the retinol-binding protein 4, also known as RBP4, in the bloodstream. RBP4 is present in much higher levels in the bodies of those with greater amounts of deep belly fat. Not only does this mean that testing for high levels of RBP4 could be useful in assessing risk for conditions such as Type 2 diabetes or heart disease, it also opens up the possibility of treating such conditions by somehow manipulating RBP4 levels.

The study in question was conducted by scientist Barbara Kahn and colleagues from Harvard Medical School, Beth Israel Deaconess Medical Center, and the University of Leipzig, Germany. The results have been published in the journal Cell Metabolism (July, 2007). Kahn is particularly well known in the area of diabetes-related research for her work on insulin resistance in mice.

There has been some very exciting news lately about the benefits of a type of pumpkin. The pumpkin is shown to slow the destruction of beta cells and reduces the need for Type 1 diabetics to inject as much insulin.

The exciting thing is that this experiment found the benefits of the pumpkin were through oral consumption, not injection. The protective effect of pumpkin is thought to be due to both antioxidants and D-chiro-inositol, a molecule that mediates insulin activity. Boosting insulin levels has the effect of lowering blood sugar levels, which reduces levels of oxidative oxygen species that damage beta-cell membranes, preventing further damage and allowing for some regeneration. Beta cells levels in the diabetic rats are, however, unlikely ever to reach that of controls, because some of the cells will have been damaged beyond repair.

An ingredient expert pointed out to me that the pumpkin used in the study is not your canned pumpkin but a special variety of Asian pumpkin. You can check at you local Asian market if they have the Shark Fin pumpkin or if they can get it for you. He also surmised that it may be possible to parlay this breed of pumpkin into a whole new world of Health Foods.

Looks like 'shrooms might become a swanky and healthy thing to do! The fungi is affectionately called the Maitake mushroom, and literally means "dancing mushroom. Research has found it lowers blood pressure, abdominal obesity, and lipids in the blood.

Maitake Products plans to target the maitake (grifola frondosa) mushroom to treat metabolic syndrome. Metabolic syndrome is a common precondition for both coronary disease and type 2 diabetes. The condition is characterized by a group of metabolic risk factors including: abdominal obesity, atherogenic dyslipidemia, high blood pressure and insulin resistance. With the growing number of people affected by these conditions, Maitake claims there is significant market potential for its drug, SX-Fraction.

A preliminary clinical study was conducted among 19 patients with type 2 diabetes. Patients taking 9 tablets of SX-Fraction (per day) for 2 months found that it significantly reduced fasting blood glucose, triglycerides, and body weight. The possibility of maitake mushroom as a safe, natural agent for treatment of type 2 diabetes, Syndrome X and insulin resistance has been examined for the past several years and will soon prove to be a therapeutic dancing mushroom in days to come. Yeah man.

Studies found that cocoa butter might be better for diabetics than other fats. A manufacturer of cocoa and chocolate is exploring the health benefits of cocoa butter for diabetics.

The positive effect of cocoa butter on diabetes was discovered during a study to determine why men and women are affected differently by diabetes. The study tried to create insulin resistance in male and female rats by feeding them a diet rich in different kinds of fats. To everyone's surprise, the animals on a cocoa fat diet developed better insulin sensitivity than those fed with other kinds of fat. Other studies have looked at the flavanoids in dark chocolate for their blood pressure lowering and insulin sensitizing attributes, so this isn't the first time chocolate seemed to have sweet effects on diabetes.

Barry Callebaut is funding this research aimed at discovering the component in cocoa butter responsible for an improvement in insulin sensitivity, with the ultimate aim of developing chocolate products for diabetics. The company has not revealed the amount of funding it is providing for the trial, nor an anticipated timeline for resulting products to be available. The positive results for the first trail - which NutraIngredients.com has not seen in full - appear to have been a surprise for those involved.

Central obesity is associated with insulin resistance through factors that are not fully understood. Researchers studied the effects of three different diets on body fat distribution, insulin sensitivity and peripheral adiponectin gene expression.

Adiponectin is secreted from fat tissue into the blood. The presence of adiponectin can result in improved insulin sensitivity and glucose tolerance, and can assist in mobilizing sugar out of the blood The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis and non-alcoholic fatty liver disease.

The study involved 11 volunteers who were the offspring of obese type 2 diabetic patients with noticeable abdominal fat deposits. The volunteers were considered insulin resistant and they maintained average hemoglobin A1c levels of greater than 6.5% without medication. All subjects underwent three dietary periods of 28 days each in a crossover design: a) diet enriched in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrates (CHO). Weight, body composition and resting energy expenditure remained unchanged during the three dietary periods. However, when patients were fed a CHO-enriched diet their fat mass was redistributed towards their abdominal region and their periphery fat accumulation decreased compared with a diet MUFA-rich and high SAT diets. Changes in fat deposition were associated with decreased levels of adiponectin after meals and lower insulin sensitivity.

The results of this study conclude a diet rich in monounsaturated fat prevents central fat redistribution and a decrease in after meal adiponectin levels. These findings support the belief that a carbohydrate-rich diet in insulin-resistant subjects exacerbates the insulin resistance. The moral of the story is: to enhance insulin sensitivity - look for a diet rich in monounsaturated fats and less dense in carbohydrates. Chances are if you've tinkered around with your food pyramid - you already knew the results of this study.

Until recently, little evidence existed regarding the effects of soy consumption on the metabolic syndrome in humans. Researchers evaluated the effects of soy consumption on metabolic symdrome and found it improved glycemic control and lipid profiles in postmenopausal women.

The study evaluated the plasma lipids, lipoproteins, insulin resistance, and glycemic control in 42 postmenopausal women with the metabolic syndrome. Participants were randomly assigned to consume a control diet (Dietary Approaches to Stop Hypertension, DASH), a soy-protein diet, or a soy-nut diet, each for 8 weeks. Red meat in the DASH period was replaced by soy-protein in the soy-protein period and by soy-nut in the soy-nut period.

The soy-nut regimen decreased the insulin resistance score significantly compared with the soy-protein or control diets. Consumption of soy-nut also reduced fasting blood sugar significantly than did the soy-protein or control diet. The soy-nut regimen decreased LDL cholesterol more than did the soy-protein period and the control diet. Soy-nut consumption significantly reduced serum C-peptide concentrations compared with control diet but consumption of soy-protein did not.

Consumption of the soy-nut leg of the experiment significantly reduced C-peptide concentrations because it was evident that the diabetic women were not creating as much insulin to counter the sugar rise in their blood. C-peptide is ONLY present when your body is producing insulin. So can one logically deduce that naturally occurring insulin causes insulin resistance? Uh oh. Sounds like we've got a pickle of a situation happening here.

Could it be that social evolution has made vitamin D deficiency a necessary evil? Studies have shown favorable effects on insulin secretion and insulin resistance in type 2 diabetic patients who received vitamin D3 supplementation.

The study evaluated 10 females with type 2 diabetes. The patients enrolled in the study treated their diabetes with oral medications. The study was conducted in March, when levels of vitamin D are lowest due to lack of sunlight. A group of 17 females with normal glucose tolerance served as a control group. The diabetic patients were treated for a month with vitamin D3. After the month, the patient's receiving vitamin D3 had increased their insulin secretion levels significantly by 34.3%. The results showed a decrease of 21.4% in insulin resistance after one month of vitamin D3 supplementation.

Back in the day, our ancestors would have full body exposure to the sun throughout the year. Nowadays, that number has been reduced to a mere 5% with only our face and hands acting as a welcome mat for the sun. A major source of vitamin D is its production in our skin as a result of UV exposure from sunlight. Lest we not take Mother Nature's generosity for granted. Everybody looks good with a little color. It'll look even better when your A1c drops as your sun-kissed glow picks up. If all else fails - you can always run off to a nudist colony where social reservations and clothing are optional!

Knocking out the gene for a peptide associated with insulin was shown to protect mice against the harmful effects of a high-fat diet. Urocortin 3 plays a role in the increased production of insulin in response to high caloric intake in animals.

Scientists found that by removing the urocortin 3 gene from mice, they did not develop the age-related insulin resistance and high blood sugar observed in the normal control mice. The metabolisms of normal mice were compared to the metabolisms of those without the urocortin 3 gene. When placed on a high caloric diet for three months, the mice without the urocortin 3 gene packed on the same amount of weight but had lower insulin levels. But these mice also had lower blood sugar, improved glucose tolerance curves and they did not develop the fatty livers the control mice experienced.

Scientists hypothesize that by curtailing the abnormally high insulin levels, they were able to manipulate insulin sensitivity and avoid some of the untoward consequences of the high food intake and weight gain. Like many of us diabetics already know too well - while insulin is effective at lowering blood sugar it also promotes fat storage. This is a natural protective response to prepare for times when food may not be available. When insulin is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organs.

Urocortin 2 and urocortin 3 are part of the system that governs the body's response to insulin. Scientists already know that mice on a high-fat diet do better if either urocortin 2 or urocortin 3 is removed. Now they want to know if the mice will respond even better if both are missing. Such results may instruct us how best to develop therapeutic means to exploit these powerful effects.

Researchers found that the type of body fat an individual has -- - white and brown-- may explain why one person gains weight easier than another.

White fat is the more familiar form of fat that accumulates in the abdomen, thighs, and buttocks. Brown fat burns energy and generates heat. White fat is deposited around internal organs and as visceral fat - the most harmful form of abdominal fat. Brown fat contains small lipid droplets tucked behind tiny energy factories called mitochondria. These cells are most prevalent in cute, little chubby babies, but tend to mostly disappear by adulthood. A 2005 Joslin study discovered genes that control the creation of the precursor cells that give rise to brown fat cells. This latest study shows that brown fat may not disappear in all adult animals and that little collections of brown fat may account for why some mice are protected from obesity and diabetes and others are not.

This study compared the difference in fat metabolism between the B6 mouse and the 129 mouse. The B6 mouse is one of the most commonly used strains in metabolic research and an established model for diet-induced obesity. When placed on a high-fat diet, the B6 mouse develops severe obesity, high blood glucose and insulin resistance with extremely high insulin levels. By contrast, the 129 mouse gains 30% to 50% less weight than the B6 mouse and is resistant to dietary induced obesity and glucose intolerance.

The only difference between the B6 and 129 mice is the type of body fat. The B6 mice had a majority of white fat cells, whereas the 129 mice had over 100 times the number of brown fat cells than the B6 mice. The mice with more white fat cells had a tendency to gain weight and develop diabetes on a high-fat diet. The study showed that the 129 mice had higher basal energy expenditure than the B6 mouse, resulting in a mitigated response to dietary effects. So I guess this begs the question -- how does one turn white fat into brown fat?

New research shows that snoring doesn't have to be loud to cause health problems especially in women. Although women generally snore less and more softly than men, recent studies have shown women have a greater risk of some of the adverse effects of sleep apnoea and may not know they have type 2 diabetes.

Sleep apnoea historically has been a problem most associated with men. However, this new research reveals that women who experience sleep apnoea may have a greater risk for developing type 2 diabetes. Both, men and women, with sleep apnoea also tend to have risk factors for the metabolic syndrome, a condition characterized by abdominal obesity, high cholesterol, raised blood pressure and insulin resistance, which causes high levels of blood glucose and can lead to diabetes.

Here comes the rude awakening -- partners of men who snore seem to be more affected by the sleep apnoea. This is due to the fact that a man's snoring is characterized by louder gasps and snorts This keeps him awake, as well as anybody within earshot. However, because women's snoring is often much quieter and they tend to have partial or incomplete obstructions, their partner's sleep may not be disturbed and the sleep disorder may go unchecked. Now I lay me down to sleep, I beg of You the silence keeps!!

According to scientists at Washington University School of Medicine in St. Louis, interrupting nerve signals to the liver can prevent diabetes and hypertension in mice.

Mice were treated to become diabetic with glucocorticoids, a class of steroid hormones characterized by an ability to bind with the cortisol receptor. Once diabetes was established, the researchers surgically removed the vagus nerve. The vagus nerve is the only nerve that starts in the brainstem and extends all the way down to the abdomen. More impressive is the fact that once the nerve was removed from the diabetic mice, insulin resistance and high blood pressure was prevented or reversed. This is an interesting discovery because people with asthma, arthritis, and organ transplants often rely on steroid treatments. It just so happens that many of them go on to develop insulin resistance.

Don't go ripping your vagus nerve out just yet. A fun fact about the vagus nerve is that it's name is taken from the Latin word meaning "wanderer". The vagal nerve pathway can influence seizures, depression and other disorders. Although the research is thoroughly enlightening, it is still very green. Hang on to your vagus nerve while the research continues.

According to research conducted by Ohio State University, conjugated linoleic acid (CLA) may help reduce body fat, but it also increases your risk for nonalcoholic fatty liver disease.

In 2003, a study showed that a 2 month supplementation of CLA lowered body mass and blood sugars in diabetics. The recent studies conducted on mice fed a CLA supplemented diet lost weight very fast, but also accumulated excessive amounts of fat in their livers - a side effect of rapid weight loss. In addition, excessive accumulation of fat in the liver is associated with insulin resistance, a factor exacerbating type 2 diabetes.

Although the recent findings were conducted on mice, CLA may or may not have a similar effect on humans. CLA has been a hot selling item in supplement stores for years. I wonder what the results would be if people who have taken CLA (the t10c12 variety) for years were to discontinue use for 4 weeks. I would be curious to see the baseline and follow-up tests for body mass, insulin sensitivity and fat accumulation in the liver. Any med students out there interested in setting-up a lab profiling hepatic function in CLA poppers?