ABSTRACT
Excessive consumption of fructose, the sweetest of all naturally occurring carbohydrates, has been linked to worldwide epidemics of metabolic diseases in humans, and it is considered an independent risk factor for cardiovascular diseases. We provide an overview about the features of fructose metabolism, as well as potential mechanisms by which excessive fructose intake is associated with the pathogenesis of metabolic diseases both in humans and rodents. To accomplish this aim, we focus on illuminating the cellular and molecular mechanisms of fructose metabolism as well as its signaling effects on metabolic and cardiovascular homeostasis in health and disease, highlighting the role of carbohydrate-responsive element-binding protein in regulating fructose metabolism.
Subject(s)
Humans , Fructose/adverse effects , Homeostasis , Metabolic Diseases/etiologyABSTRACT
AIM: To demonstrate the changes of activity and electron microscopic enzyme cytochemistry staining of H+-K+-ATPase of gastric parietal cells under stress in rats.METHODS: Twenty-four male SD rats were randomly divided into normal group,stress group and stress+omeprazole(OM) group.Water immersion-restraint stress(WRS) model in SD rats was performed.The ulcer index(UI) of gastric mucosa and H+-K+-ATPase activity of gastric parietal cells were measured.The changes of ultrastructure and electron microscopic enzyme cytochemistry staining of parietal cells were observed under transmission electron microscope(TEM).RESULTS: Compared with control group,the UI of gastric mucosa and H+-K+-ATPase activity of gastric parietal cells increased(P
