Tampilkan postingan dengan label REDUCES. Tampilkan semua postingan
Tampilkan postingan dengan label REDUCES. Tampilkan semua postingan

Jumat, 25 Agustus 2017

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.

Selasa, 01 Agustus 2017

NICOTINE WITHDRAWAL REDUCES RESPONSE TO REWARDS ACROSS SPECIES



Cigarette smoking is a leading cause of preventable death worldwide and is associated with approximately 440,000 deaths in the United States each year, according to the U.S. Centers for Disease Control and Prevention, but nearly 20 percent of the U.S. population continues to smoke cigarettes. While more than half of U.S. smokers try to quit every year, less than 10 percent are able to remain smoke-free, and relapse commonly occurs within 48 hours of smoking cessation. Learning about withdrawal and difficulty of quitting can lead to more effective treatments to help smokers quit.

In a first of its kind study on nicotine addiction, scientists measured a behavior that can be similarly quantified across species like humans and rats, the responses to rewards during nicotine withdrawal. Findings from this study were published online on Sept. 10, 2014 in JAMA Psychiatry.

Response to reward is the brain's ability to derive and recognize pleasure from natural things such as food, money and sex. The reduced ability to respond to rewards is a behavioral process associated with depression in humans. In prior studies of nicotine withdrawal, investigators used very different behavioral measurements across humans and rats, limiting our understanding of this important brain reward system.
Using a translational behavioral approach, Michele Pergadia, Ph.D., associate professor of clinical biomedical science in the Charles E. Schmidt College of Medicine at Florida Atlantic University, who completed the human study while at Washington University School of Medicine, Andre Der-Avakian, Ph.D., who completed the rat study at the University of California San Diego (UCSD), and colleagues, including senior collaborators Athina Markou, Ph.D. at UCSD and Diego Pizzagalli, Ph.D. at Harvard Medical School, found that nicotine withdrawal similarly reduced reward responsiveness in human smokers -- particularly those with a history of depression -- as well as in nicotine-treated rats.
Pergadia, one of the lead authors, notes that replication of experimental results across species is a major step forward, because it allows for greater generalizability and a more reliable means for identifying behavioral and neurobiological mechanisms that explain the complicated behavior of nicotine withdrawal in humans addicted to tobacco.

"The fact that the effect was similar across species using this translational task not only provides us with a ready framework to proceed with additional research to better understand the mechanisms underlying withdrawal of nicotine, and potentially new treatment development, but it also makes us feel more confident that we are actually studying the same behavior in humans and rats as the studies move forward," said Pergadia.

Pergadia and colleagues plan to pursue future studies that will include a systematic study of depression vulnerability as it relates to reward sensitivity, the course of withdrawal-related reward deficits, including effects on relapse to smoking, and identification of processes in the brain that lead to these behaviors.
Pergadia emphasizes that the ultimate goal of this line of research is to improve treatments that manage nicotine withdrawal-related symptoms and thereby increase success during efforts to quit.
"Many smokers are struggling to quit, and there is a real need to develop new strategies to aid them in this process. Therapies targeting this reward dysfunction during withdrawal may prove to be useful," said Pergadia.


Minggu, 13 November 2016

RESEARCHERS IDENTIFY PEPTIDE THAT REDUCES URGE TO EAT



Researchers have identified a peptide and hormone that when administered to a specific area of the brain may reduce the desire for food. The study, which appears in the journalNeuropsychopharmacology, may one day lead to medications that treat obesity and binge eating disorders
Obesity is a complex disorder affecting more than 78 million Americans which involves an excessive amount of body fat. It increases your risk of diseases and health problems such as heart disease, diabetes and high blood pressure. Binge-eating disorder is a prevalent illness in America characterized by periods of excessive uncontrolled consumption of food, followed by uncomfortable fullness and feelings of self-disgust.
Using an experimental model, the researchers found when administering pituitary adenylate cyclase-activating peptide (PACAP), a peptide and hormone produced by neurons, in a specific area of the brain called the "central amygdala," it reduced the intake of food and led to weight loss.
According to the researchers PACAP is known for its food intake and body weight effects in the hypothalamus (the area of the brain known for controlling appetite). However, this is the first report of PACAP effects in the amygdala, a region of the brain outside the hypothalamus, involved in fear but also in the emotional component of eating.
The researchers also discovered how PACAP decreases food intake when injected in the amygdala. In general, food intake can be decreased in two ways: eating fewer meals of normal size during the day, or smaller meals. "We found that amygdalar PACAP reduces the amount of food eaten within meals, but not how many meals are consumed. In addition, we found that PACAP reduced the rate of intake of food. This means that, following administration of PACAP, models were eating more slowly," explained Valentina Sabino, PhD, assistant professor of pharmacology and psychiatry, and co-director of the Laboratory of Addictive Disorder at Boston University School of Medicine (BUSM).
In addition, they found that PACAP effects on food intake and body weight were dependent on another brain factor: the growth-hormone called brain-derived neurotrophic factor (BDNF). "The effects of PACAP on food intake and body weight were absent when it was given together with another drug that blocks BDNF signaling, suggesting that PACAP acts through BDNF," said Sabino.
The researchers believe these findings have implications for a variety of conditions, since they found not only how much food subjects ate but also how fast they ate them. "The PACAP system may hypothetically be the target of medications to treat not only obesity but also binge-eating, a disease characterized by excessive, uncontrollable consumption of food within brief periods of time," added coauthor Pietro Cottone, PhD, associate professor of pharmacology and psychiatry and co-director of the Laboratory of Addictive Disorder at BUSM.
Also contributing to this study were BU researchers: Attilio Iemolo, PhD, and Antonio Ferragud, MS.
Funding for this study was provided by the National Institute of Health (National Institute of Mental Health and National Institute on Drug Abuse), the Peter Paul Career Development Professorship, the Peter McManus Charitable Trust, and Boston University's Undergraduate Research Opportunities Program (UROP).