HEALING THE HEART WITH FAT

Too much dietary fat is bad for the heart, but the right kind of fat keeps the heart healthy, according to a paper published in The Journal of Experimental Medicine.

Unsaturated dietary fatty acids, such as eicosapentaenoic acid (EPA), are known to protect against cardiovascular diseases. However, the mechanism and the specific fat metabolites responsible for this protection were unknown.

A group of Japanese scientists now show that mice engineered to produce their own EPA are protected against heart disease and have improved cardiac function. One particular EPA metabolite, called 18-hydroxyeicosapentaenoic acid (18-HEPE), was required for this protection.

18-HEPE was produced by immune cells called macrophages, which dampened inflammation and fibrosis in the heart. Treatment with 18-HEPE confirmed its heart-protective effects.

A diet enriched in 18-HEPE might thus help prevent heart failure in patients with cardiovascular diseases.

HIGH SALT PREVENTS WEIGHT GAIN IN MICE ON A HIGH FAT DIET

In a study that seems to defy conventional dietary wisdom, University of Iowa scientists have found that adding high salt to a high-fat diet actually prevents weight gain in mice.

As exciting as this may sound to fast food lovers, the researchers caution that very high levels of dietary salt are associated with increased risk for cardiovascular disease in humans. Rather than suggest that a high salt diet is suddenly a good thing, the researchers say these findings really point to the profound effect non-caloric dietary nutrients can have on energy balance and weight gain.

"People focus on how much fat or sugar is in the food they eat, but [in our experiments] something that has nothing to do with caloric content -- sodium -- has an even bigger effect on weight gain," say Justin Grobe, PhD, assistant professor of pharmacology at the UI Carver College of Medicine and co-senior author of the study, which was published in the journalScientific Reports on June 11.

The UI team started the study with the hypothesis that fat and salt, both being tasty to humans, would act together to increase food consumption and promote weight gain. They tested the idea by feeding groups of mice different diets: normal chow or high-fat chow with varying levels of salt (0.25 to 4 percent). To their surprise, the mice on the high-fat diet with the lowest salt gained the most weight, about 15 grams over 16 weeks, while animals on the high-fat, highest salt diet had low weight gain that was similar to the chow-fed mice, about 5 grams.

"We found out that our 'french fry' hypothesis was perfectly wrong," says Grobe, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and a Fellow of the American Heart Association. "The findings also suggest that public health efforts to continue lowering sodium intake may have unexpected and unintended consequences."

To investigate why the high salt prevented weight gain, the researchers examined four key factors that influence energy balance in animals. On the energy input side, they ruled out changes in feeding behavior -- all the mice ate the same amount of calories regardless of the salt content in their diet. On the energy output side, there was no difference in resting metabolism or physical activity between the mice on different diets. In contrast, varying levels of salt had a significant effect on digestive efficiency -- the amount of fat from the diet that is absorbed by the body.

"Our study shows that not all calories are created equal," says Michael Lutter, MD, PhD, co-senior study author and UI assistant professor of psychiatry. "Our findings, in conjunction with other studies, are showing that there is a wide range of dietary efficiency, or absorption of calories, in the populations, and that may contribute to resistance or sensitivity to weight gain."

"This suppression of weight gain with increased sodium was due entirely to a reduced efficiency of the digestive tract to extract calories from the food that was consumed," explains Grobe.

It's possible that this finding explains the well-known digestive ill effects of certain fast foods that are high in both fat and salt, he adds.

Through his research on hypertension, Grobe knew that salt levels affect the activity of an enzyme called renin, which is a component in the renin- angiotensin system, a hormone system commonly targeted clinically to treat various cardiovascular diseases. The new study shows that angiotensin mediates the control of digestive efficiency by dietary sodium.

The clinical usefulness of reducing digestive efficiency for treating obesity has been proven by the drug orlistat, which is sold over-the-counter as Alli. The discovery that modulating the renin-angiotensin system also reduces digestive efficiency may lead to the developments of new anti-obesity treatments.

Lutter, who also is an eating disorders specialist with UI Health Care, notes that another big implication of the findings is that we are just starting to understand complex interactions between nutrients and how they affect calorie absorption, and it is important for scientists investigating the health effects of diet to analyze diets that are more complex than those currently used in animal experiments and more accurately reflect normal eating behavior.

"Most importantly, these findings support continued and nuanced discussions of public policies regarding dietary nutrient recommendations," Grobe adds.

In addition to Grobe and Lutter, the UI research team included Benjamin Weidemann; Susan Voong; Fabiola Morales-Santiago; Michael Kahn; Jonathan Ni; Nicole Littlejohn; Kristin Claflin; Colin Burnett; and Nicole Pearson. The study was funded in part by grants from the National Heart, Lung and Blood Institute, the American Diabetes Association, and American Heart Association.

HUNGER GAMES HOW THE BRAIN BROWNS FAT TO AID WEIGHT LOSS

Researchers at Yale School of Medicine have uncovered a molecular process in the brain known to control eating that transforms white fat into brown fat. This process impacts how much energy we burn and how much weight we can lose. The results are published in the Oct. 9 issue of the journal Cell.

Obesity is a rising global epidemic. Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues, which are made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat. The more brown fat you have, the more weight you can lose.

It has previously been shown that energy-storing white fat has the capacity to transform into energy-burning "brown-like" fat. In this new study, researchers from the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism, demonstrate that neurons controlling hunger and appetite in the brain control the "browning" of white fat.

Lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine, conducted the study with Tamas Horvath, professor and chair of comparative medicine, and professor of neurobiology and Obstetrics/gynecology at Yale School of Medicine, and their co-authors.

The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called "O-GlcNAc" to potassium ion channels acts as a switch to control brain activity to burn fat.

"Our studies reveal white fat "browning" as a highly dynamic physiological process that the brain controls," said Yang. "This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned."

Yang said hunger and cold exposure are two life-history variables during the development and evolution of mammals. "We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry. Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses."

FAT TONGUE LINKED TO SLEEP APNEA RISK

Obese adults with a significantly larger tongue and higher percentage of fat are more likely to develop obstructive sleep apnea than others, says a study.

Common warning signs for sleep apnea include snoring and choking, gasping, or silent breathing pauses during sleep.

Obese adults with sleep apnea had significantly greater tongue volumes, tongue fat and percentage of tongue fat than obese controls without sleep apneea, the findings showed.

"This is the first study to show that fat deposits are increased in the tongue of obese patients with obstructive sleep apnea," said principal investigator Richard Schwab, a professor at University of Pennsylvania Medical Center in Philadelphia, US.

Further analysis found that tongue fat percentage in participants with sleep apnea was site-specific, with increased fat toward the base of the tongue in the retroglossal region

"Tongue size is one of the physical features that should be evaluated by a physician when screening obese patients to determine their risk for obstructive sleep apnea," said Timothy Morgenthaler, president, American Academy of Sleep Medicine.

The study involved 90 obese adults with sleep apnea and 31 obese controls without sleep apnea.

All participants underwent high resolution upper airway magnetic resonance imaging (MRI).

In addition to enlarging the size of the tongue, increased tongue fat may impair the functioning of the muscles that attach the tongue to the bone, preventing these muscles from positioning the tongue away from the airway, the authors proposed.

The study appeared in the journal Sleep.

HUMAN MILK FAT IMPROVES GROWTH IN PREMATURE INFANTS

For premature infants, adequate growth while in the neonatal intensive care unit is an indicator of better long-term health and developmental outcomes. Researchers at the USDA/ARS Children's Nutrition Research Center at Baylor College of Medicine and Texas Children's Hospital have now successfully incorporated a cream supplement into premature infants' diets that improved their growth outcomes in the NICU. The report appears in the Journal of Pediatrics

For premature babies who weigh less than 1,000 grams (about 2 pounds, 2 ounces), one of the problems is that their lungs and other organs are still developing when they are born. If the infant gains weight and increases in length at a good rate while in the NICU, this helps improve their outcomes," said Dr. Amy Hair, assistant professor of pediatrics at Baylor, neonatologist at Texas Children's Hospital and first author of the study.

Previous research has shown that an exclusive human milk diet protects the intestines of premature infants and supports their growth. This diet consists of mothers' own breast milk or donor human milk, as well as a fortifier consisting of protein and minerals made from the donor milk.

In this study, researchers sought a way to optimize this growth in very small infants (those who weigh between 750 and 1,250 grams) who need additional calories. Because infants are already receiving enough protein from the fortifier, another way to help them grow is by giving them fat. One of the byproducts of pasteurizing donor milk is milk fat, also referred to as a cream supplement.

In this study, researchers compared the growth outcomes of infants who received the exclusive human milk diet and the cream supplement to infants who received just the exclusive human milk diet. They found that infants in the cream group had better growth outcomes in terms of weight and length than infants in the control group.

"This is a natural way to give them fat. Previously, we would add oils or infant formula to help premature babies grow, but we can now use a natural source from donor milk," said Hair.

Hair noted that because the growth was both in weight and length, this growth is likely lean mass, consisting of bone and muscle growth.

"You want to see babies growing in both weight and length," said Hair.

She also noted that the volume of milk given to these infants cannot change to help them grow because their stomach and intestine can only tolerate a certain amount of feedings.

"You cannot give them more volumes of milk. Especially if they have lung problems, they have to have a certain volume of milk. This is a way to add calories but not change the volume of milk," she said.

Since November 2013, the NICU at Texas Children's Hospital has changed its protocol to add this cream supplement to the diet of infants who weigh less than 1,500 grams.

"This also emphasizes the importance of donating excess breast milk that your baby doesn't need to a milk bank. It can help nourish our tiniest and most vulnerable infants," said Hair.

Texas Children's was the first hospital in the world to add human milk-based cream to the diets of very low birth weight infants.

In addition to adding cream to the diets of premature infants, since 2009, Texas Children's has significantly reduced its rates of necrotizing enterocolitis, one of the most devastating and potentially fatal diseases a neonate can face, by implementing a human milk feeding protocol for all infants weighing less than 3.3 pounds.

"Texas Children's strives to be a leader in human milk feeding, because we know it impacts outcomes," said Hair.