Researchers interested in determining the direct effects of a high saturated fat and high cholesterol (HFHC) diet on implanted fetal hippocampal tissues have found that in middle-aged laboratory rats the HFHC diet elevated microglial activation and reduced neuronal development. While the resulting damage was due to an inflammatory response in the central nervous system, they found that the effects of the HFHC diet were alleviated by the interleukin (IL)-1 receptor antagonist IL-1Ra, leading them to conclude that IL-Ra has potential use in neurological disorders involving neuroinflammation. They published their results in a recent issue of Cell Transplantation (20:10), now freely available on-line.* To carry out the study, the researchers transplanted hippocampal grafts from embryonic 18 day-old rats into the anterior eye chambers of 16-month old host animals that were subsequently fed either a normal rat chow diet or a HFHC diet for eight weeks.
In a study published in Nutrition Research, researchers looked at the association of out-of-hand nut (OOHN) consumption with nutrient intake, diet quality and the prevalence of risk factors for cardiovascular disease and metabolic syndrome in both children and adults. Consumers of OOHN, including tree nuts (almonds, Brazil nuts, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts), had higher intakes of energy, monounsaturated and polyunsaturated fats (the good fats) and dietary fiber, and lower intakes of carbohydrates, cholesterol and sodium than non-consumers. "Adult consumers also had a 19% decreased risk of hypertension and a 21% decreased risk of low high-density lipoprotein (HDL - -the good cholesterol) levels - both risk factors for metabolic syndrome and cardiovascular disease, " stated Carol O'Neil, PhD, MPH, RD, lead author on the paper and Professor at Louisiana State University Agricultural Center.
Niacin, or vitamin B3, is the one approved drug that elevates "good" cholesterol (high density lipoprotein, HDL) while depressing "bad" cholesterol (low density lipoprotein, LDL), and has thereby attracted much attention from patients and physicians. Niacin keeps fat from breaking down, and so obstructs the availability of LDL building blocks. Patients often stop taking niacin because it causes uncomfortable facial flushing, an effect caused by the release of a fat called prostaglandin or (PG)D2. PGD2 is the primary cause of the unwanted vasodilation, the "niacin flush." The dilation occurs when blood vessels widen from relaxed smooth muscle cells within vessel walls. PGD2, formed by an enzyme called COX-2 and released by immune and skin cells, acts on a muscle cell-surface receptor called DP1 to cause the flushing.
Alzheimer's disease (AD) is now the sixth leading cause of death among Americans, affecting nearly 1 in 8 people over the age of 65. There is currently no treatment that alters the course of this disease. However, an increasing amount of evidence suggests that changes in the way the body handles iron and other metals like copper and zinc may start years before the onset of AD symptoms. A new study shows that reducing iron levels in blood plasma may protect the brain from changes related to AD. In the current study a group of investigators from led by Dr. Othman Ghribi, PhD, Associate Professor, Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine and Health Sciences, rabbits were fed a high-cholesterol diet which caused them to accumulate plaques of a small protein called beta-amyloid (AÎ ).
Removing a lipoprotein receptor known as SR-BI may help protect against breast cancer, as suggested by new findings presented at the American Association for Cancer Research Annual Meeting 2012 by Jefferson's Kimmel Cancer Center researchers. In vitro and mouse studies revealed that depletion of the SR-BI resulted in a decrease in breast cancer cell growth. SR-BI is a receptor for high-density lipoproteins (HDL) that are commonly referred to as "good cholesterol " because they help transport cholesterol out of the arteries and back to the liver for excretion. The team, including Christiane Danilo, of the Department Stem Cell Biology and Regenerative Medicine at Thomas Jefferson University, and Philippe G. Frank, Ph.D., an assistant professor in the Department of Stem Cell Biology and Regenerative Medicine at Jefferson, had good reason to believe that SR-BI played a role in breast cancer growth: Previous lab research had revealed that mice fed a high cholesterol diet develop more advanced tumors and their tumors produce more SR-BI.