Coffee and tea may contribute to a healthy liver

Aug. 16, 2013 — Surprise! Your morning cup of tea or coffee may be doing more than just perking you up before work.An international team of researchers led by Duke-NUS Graduate Medical School (Duke-NUS) and the Duke University School of Medicine suggest that increased caffeine intake may reduce fatty liver in people with non-alcoholic fatty liver disease (NAFLD).Worldwide, 70 percent of people diagnosed with diabetes and obesity have NAFLD, the major cause of fatty liver not due to excessive alcohol consumption. It is estimated that 30 percent of adults in the United States have this condition, and its prevalence is rising in Singapore. There are no effective treatments for NAFLD except diet and exercise.Using cell culture and mouse models, the study authors — led by Paul Yen, M.D., associate professor and research fellow, and Rohit Sinha, Ph.D of the Duke-NUS Graduate Medical School’s Cardiovascular and Metabolic Disorders Program in Singapore — observed that caffeine stimulates the metabolization of lipids stored in liver cells and decreased the fatty liver of mice that were fed a high-fat diet. These findings suggest that consuming the equivalent caffeine intake of four cups of coffee or tea a day may be beneficial in preventing and protecting against the progression of NAFLD in humans.The findings will be published in the September issue of the journal Hepatology.”This is the first detailed study of the mechanism for caffeine action on lipids in liver and the results are very interesting,” Yen said. “Coffee and tea are so commonly consumed and the notion that they may be therapeutic, especially since they have a reputation for being “bad” for health, is especially enlightening.”The team said this research could lead to the development of caffeine-like drugs that do not have the usual side effects related to caffeine, but retain its therapeutic effects on the liver. It could serve as a starting point for studies on the full benefits of caffeine and related therapeutics in humans.In addition to Yen and Sinha, collaborators included Christopher Newgard, PhD, director of the Sarah W. Stedman Nutrition and Metabolism Center at Duke University School of Medicine, where the metabolomics analysis of the data was conducted.The study was supported by funding from Singapore’s Agency for Science, Technology, and Research; the Ministry of Health; and the Ministry of Education.

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High-fat diet during pregnancy contributes to offspring’s increased weight

June 17, 2013 — Exposure to a high-fat diet in the womb and after birth can permanently change the cells in the brain that control food intake, predisposing monkeys to overeating and an increased preference for fatty and sugary foods, a new study finds.The results were presented Monday at The Endocrine Society’s 95th Annual Meeting in San Francisco.The study, funded by the National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases, also found that male offspring of maternal monkeys that ate a high-fat diet had increased body weight, compared with the offspring of mothers that ate a low-fat diet.”Studies in humans have demonstrated that maternal obesity during pregnancy is a strong determinant of offspring body mass index, or BMI,” said the study’s lead author, Juliana Gastao Franco, PhD, a postdoctoral fellow at Oregon Health and Science University.”Our group demonstrated that consumption of a high-fat diet during gestation alters fetal development of neurons that control food intake, ultimately leading to an increased preference for high-calorie food and to increased body fat in the offspring.”Franco and her co-investigators studied monkeys born to females that consumed either a low-fat (control) diet, consisting of 14 percent of calories from fat, or a high-fat diet in which 36 percent of calories came from fat. After weaning, 20 offspring of female monkeys on the high-fat diet either received the same high-fat diet (8 monkeys) or were switched to the control diet (12 monkeys). Seven offspring of the control monkeys continued to receive the control diet.When the monkeys were 6 to 11 months of age (equivalent to toddlers in humans), the researchers measured their total food intake, dietary preferences, body composition, physical activity and metabolic rate, which is the rate at which the body burns calories. Using molecular and cell biology techniques, the investigators examined neurotransmitter systems in the monkeys’ hypothalamus, the region of the brain that regulates food intake.All male offspring that had fetal exposure to a high-fat diet had increased body weight, despite having no changes in their metabolic rate and regardless of what they ate after weaning, Franco reported. Also, the offspring that were switched to the control diet displayed, on average, greater overall food intake and increased binge eating of food with high sugar and fat, compared with either those maintained on a high-fat diet or the controls’ offspring, she said.According to Franco, these animals had what appeared to be permanent changes in their hypothalamus — an abnormal organization of the neurons that control food intake.Co-author Elinor Sullivan, PhD, also of Oregon Health and Science University, speculated on the possible cause of this neurochemical change.”We know that obesity incites inflammatory cytokines [molecules], which change how neurons develop,” Sullivan said. “We believe that inflammation in the brain is causing the reprogramming of these appetite-regulating neurons.”

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Brain circuits link obsessive-compulsive behavior and obesity

June 10, 2013 — What started as an experiment to probe brain circuits involved in compulsive behavior has revealed a surprising connection with obesity.The University of Iowa-led researchers bred mice missing a gene known to cause obesity, and suspected to also be involved in compulsive behavior, with a genetic mouse model of compulsive grooming. The unexpected result was offspring that were neither compulsive groomers nor obese.The study, published the week of June 10 in the online early edition of the Proceedings of the National Academy of Sciences (PNAS), suggests that the brain circuits that control obsessive-compulsive behavior are intertwined with circuits that control food intake and body weight. The findings have implications for treating compulsive behavior, which is associated with many forms of psychiatric disease, including obsessive-compulsive disorder (OCD), Tourette syndrome, and eating disorders.UI neuro-psychiatrists Michael Lutter, M.D., Ph.D. and Andrew Pieper, M.D., Ph.D., led the study. The team also included researchers from Stanford University School of Medicine, University of Texas Southwestern Medical Center, Beth Israel Deaconess Medical Center, and Harvard Medical School.Lutter, an assistant professor of psychiatry, and Pieper, an associate professor of psychiatry and neurology at the UI Carver College of Medicine, both recently arrived at the UI and use mouse models in their laboratories to study human disorders and conditions.Pieper is interested in compulsive behavior. His mouse model of compulsivity lacks a brain protein called SAPAP3. These mice groom themselves excessively to the point of lesioning their skin, and their compulsive behavior can be effectively treated by fluoxetine, a drug that is commonly used to treat OCD in people.Lutter works with a mouse that genetically mimics an inherited form of human obesity. This mouse lacks a brain protein known a MC4R. Mutations in the MC4R gene are the most common single-gene cause of morbid obesity and over-eating in people.“I study MC4R signaling pathways and their involvement in the development of obesity,” Lutter explains. “I’m also interested in how these same molecules affect mood and anxiety and reward, because it’s known that there is a connection between depression and anxiety and development of obesity.”An old study hinted that in addition to its role in food intake and obesity, MC4R might also play a role in compulsive behavior, which got Lutter and Pieper thinking of ways to test the possible interaction.”We knew in one mouse you could stimulate excessive grooming through this MC4R pathway and in another mouse a different pathway (SAPAP3) caused compulsive grooming,” Lutter says. …

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