CONSUMING WHEY PROTEIN BEFORE MEALS REDUCES BLOOD SUGAR SPIKES

A whey protein drink before breakfast can control erratic glucose levels associated with type 2 diabetes, say Tel Aviv University researchers

Blood sugar surges - after-meal glucose "spikes" - can be life threatening for the 29 million Americans with diabetes. Diabetic blood sugar spikes have been linked to cardiovascular disease, cancer, alzheimer’s diseases ,  , kidney failure, and retinal damage. Now a new Tel Aviv University study, published inDiabetologia, suggests a novel way to suppress these deadly post-meal glucose surges: the consumption of whey protein concentrate, found in the watery portion of milk separated from cheese curds, before breakfast.

According to TAU's Prof. Daniela Jakubowicz and Dr. Julio Wainstein of the Wolfson Medical Center's Diabetes Unit, Prof. Oren Froy of the Hebrew University of Jerusalem, and Prof. Bo Ahrén of Lund University in Sweden, the consumption of whey protein before meals may even keep diabetics' need for insulin treatment at bay.

"What's remarkable is that consuming whey protein before meals reduces the blood sugar spikes seen after meals. It also improves the body's insulin response, putting it in the same range or even higher than that produced by novel anti-diabetic drugs," said Prof. Jakubowicz. "High milk intake has long been associated with lower risk for type 2 diabetes and cardiovascular disease, and milk whey protein increases the production of a gut hormone called glucagon-like peptide-1 (GLP-1) that stimulates insulin secretion. This, in turn, reduces the blood glucose rise after meals."

"We hypothesized that stimulating GLP-1 production by consuming whey protein before a meal would enhance insulin secretion and have beneficial glucose-lowering effects in type 2 diabetes," Prof. Jakubowicz said.

The study was conducted on 15 individuals with well-controlled type 2 diabetes at Wolfson Medical Center. The participants were randomized to receive either 50 grams of whey in 250 ml water or a placebo, followed by a standardized high-glycemic index breakfast of three slices of white bread and sugary jelly - a meal designed to produce the maximum post-meal glucose spike.

Blood samples were taken 30 minutes before the meal, when the whey protein or placebo drinks were consumed. Further blood samples, assessing plasma concentration of glucose, intact GLP-1, and insulin concentrations, were taken when the breakfast was served and at 15, 30, 60, 90, 120, 150, and 180 minute intervals after the meal.

The researchers found that glucose levels were reduced by 28 percent after the whey pre-load over the 180-minute post-meal period, with a uniform reduction during early and late phases. With whey pre-load, insulin and GLP-1 responses also were significantly higher (105 and 141 percent, respectively), producing a 96 percent increase in early insulin response.

"The early insulin response that usually is deficient in type-2 diabetes was significantly higher after whey protein than with placebo, and the whey protein preload significantly reduced the elevation of blood glucose after breakfast," said Prof. Jakubowicz. "Whey protein could therefore represent a novel approach for enhancing glucose-lowering strategies in type 2 diabetes."

Based on the findings of this study, the authors are considering a long-term clinical trial to test the enduring benefits of whey protein consumption for diabetics.

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BRAIN CIRCUIT THAT THAT CONTROLS COMPULSIVE OVEREATING AND SUGAR ADDICTION DISCOVERED

Compulsive overeating and sugar addiction are major threats to human health, but potential treatments face the risk of impairing normal feeding behaviors that are crucial for survival. A study published January 29th in the journal Cell reveals a reward-related neural circuit that specifically controls compulsive sugar consumption in mice without preventing feeding necessary for survival, providing a novel target for the safe and effective treatment of compulsive overeating in humans

Although obesity and Type 2 diabetes are major problems in our society, many treatments do not tackle the primary cause: unhealthy eating habits," says senior study author Kay Tye of the Massachusetts Institute of Technology. "Our findings are exciting because they raise the possibility that we could develop a treatment that selectively curbs compulsive overeating without altering healthy eating behavior."

Compulsive overeating is a type of reward-seeking behavior, similar to drug addiction. But the major difference between the two behaviors is that eating is required for survival, underscoring the need to tease apart brain circuits involved in compulsive overeating versus normal feeding to develop safe and effective therapies. Tye and her team suspected that a neural pathway from the lateral hypothalamus to the ventral tegmental area might play an important role in compulsive overeating because these brain regions have been implicated in reward-related behaviors such as eating, sexual activity, and drug addiction.

To test this idea, Tye and her team used a technique called optogenetics, which involves genetically modifying specific populations of neurons to express light-sensitive proteins that control neural excitability, and then delivering either blue or yellow light through an optic fiber to activate or inhibit those cells, respectively. Activation of the pathway from the lateral hypothalamus to the ventral tegmental area caused well-fed mice to spend more time feeding and increased the number of times mice poked their nose into a port to receive a sugar reward, even when they had to cross a platform that delivered foot shocks to get to the reward. By contrast, inhibition of the same pathway reduced this compulsive sugar-seeking behavior without decreasing food consumption in hungry mice, suggesting that different neural circuits control feeding in hungry animals.

In an independent study also published January 29th in Cell, Garret Stuber of the University of North Carolina School of Medicine and his team similarly used an optogenetic approach in mice to identify neurons in the lateral hypothalamus that control both feeding and reward-seeking behavior. By imaging the activity of hundreds of individual lateral hypothalamus neurons as the mice freely explored an area with food or worked to obtain a sweet reward, they further uncovered distinct subsets of neurons that either mediate food-seeking behavior or respond to reward consumption.

According to Tye, it makes sense that brain circuits evolved to support binging on scarce, sugary foods whenever these valuable sources of energy become transiently available during certain seasons. But in the winter, it might be adaptive for separate neural circuits to drive hungry animals to eat whatever type of food is available but to consume less overall to ration out limited resources.

"However, in our modern day society, there is no scarcity of palatable foods, and high-sugar or high-fat foods are often even more available than fresh produce or proteins," Tye says. "We have not yet adapted to a world where there is an overabundance of sugar, so these circuits that drive us to stuff ourselves with sweets are now serving to create a new health problem. The discovery of a specific neural circuit underlying compulsive sugar consumption could pave the way for the development of targeted drug therapies to effectively treat this widespread problem."