Consuming a high-fat diet enriched with omega 6 fatty acids may increase the risk of developing diabetes to heart failure in older adults, according to scientists including one of Indian origin.
Scientists at University of Alabama at Birmingham in the US investigated how ageing and an obesity-generating omega 6-enriched diet impact microflora in the gut, the structure and function of the spleen, and a subsequent immune response to heart attack, using a mouse model. “The data strongly indicate that the obesity-generating diet develops an inflammatory micro-environment, even in young mice, that amplifies with aging,” said Ganesh Halade, an associate professor at University of Alabama at Birmingham.
“This study highlights that diet and age are critical factors that have differential impact with age, and it highlights the spleen and heart as an inter-organ communication system with the immune defense system,” Halade said. The study, published in the FASEB Journal, shows that a calorie-dense, obesity-generating diet in ageing mice disrupted the composition of the gut microbiome, and that correlated with development of a systemwide nonresolving inflammation in acute heart failure, with disruptions of the immune cell profile — notably the neutrophil-leukocyte ratio. It is known that diet interacts with gut microbes to calibrate the body’s immune defense capacity. The researchers examined this further, with regard to ageing and a high-fat diet.
They found that the obesity-generating diet caused a sharp increase in bacteria belonging to the genus Allobaculum, phylum Firmicutes. The obesity-generating diet also increased the proportion of neutrophils in the blood of young mice. In aged mice, a similar increase in the proportion of neutrophils was found for both old mice fed a standard diet and old mice fed the obesity-generating diet.
The spleen, a secondary immune organ, is a known reservoir for leukocytes that are released after heart injury. Those splenic leukocytes move to the heart to begin tissue repair and help resolve inflammation. The team found that the obesity-generating diet and ageing led to neutrophil swarming and an altered leukocyte profile after heart attack. They also observed splenic structural deformities in these mice and a decrease in splenic CD169-positive macrophages.
Importantly, young mice fed the obesity-generating diet were able to resolve inflammation after a heart attack, even though their gut microflora had already been altered by the diet. In contrast, in aged mice fed the obesity-generating diet, the heart attack triggered non-resolving inflammation. Such inflammation is associated with heart failure.