Enteric pathogens modulate metabolic homeostasis in the Drosophila melanogaster host.

On quotidian basis, living beings work out an armistice with their microbial flora and a scuffle with invading pathogens to maintain a normal state of health. Although producing virulence factors and escaping the host's immune machinery are the paramount tools used by pathogens in their "arm race" against the host; here, we provide insight into another facet of pathogenic embitterment by presenting evidence of the ability of enteric pathogens to exhibit pathogenicity through modulating metabolic homeostasis in Drosophila melanogaster. We report that Escherichia coli and Shigella sonnei orally infected flies exhibit lipid droplet deprivation from the fat body, irregular accumulation of lipid droplets in the midgut, and significant elevation of systemic glucose and triglyceride levels.

Between Inflammation and Autophagy: The Role of Leptin-Adiponectin Axis in Cardiac Remodeling.

Cardiac remodeling is the process by which the heart adapts to stressful stimuli, such as hypertension and ischemia/reperfusion; it ultimately leads to heart failure upon long-term exposure. Autophagy, a cellular catabolic process that was originally considered as a mechanism of cell death in response to detrimental stimuli, is thought to be one of the main mechanisms that controls cardiac remodeling and induces heart failure. Dysregulation of the adipokines leptin and adiponectin, which plays essential roles in lipid and glucose metabolism, and in the pathophysiology of the neuroendocrine and cardiovascular systems, has been shown to affect the autophagic response in the heart and to contribute to accelerate cardiac remodeling.

Molecular Mechanisms of Adiponectin-Induced Attenuation of Mechanical Stretch-Mediated Vascular Remodeling.

Hypertension induces vascular hypertrophy, which changes blood vessels structurally and functionally, leading to reduced tissue perfusion and further hypertension. It is also associated with dysregulated levels of the circulating adipokines leptin and adiponectin (APN). Leptin is an obesity-associated hormone that promotes vascular smooth muscle cell (VSMC) hypertrophy.