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Type 2 diabetes caused by chronic obesity is a major lifestyle-related disease. The present study aimed to determine the pathological changes in hepatocytes in chronic obesity. To develop our type 2 diabetes mouse model, we induced chronic obesity to mice by monosodium glutamate. By overeating, the mice significantly increased their body weight compared with age-matched healthy animals. To analyze the pathological changes in hepatocytes of chronic obesity before preclinical stage of type 2 diabetes, the mice were analyzed by hematoxylin-eosin staining of tissue sections at 15 w of age. In these mice, we observed eosin-negative accumulations of hepatocytes around central veins in the hepatic lobule. By Oil-Red O staining, the eosin-negative granules were identified in the lipid droplets. We then ascertained whether these lipid droplets of hepatocytes in the obese mice could be modified by diet. After 24 h of diet restriction, the lipid droplets of hepatocytes in the obese mice were swollen. Furthermore, after 48 h of the diet restriction, the lipid droplets continued swelling and the autophagy-like structures that were found in the healthy mice under the same condition in the obese mice were not observed. These results suggest that the obese mice might have delayed energy metabolism, which might have influenced the mechanisms of hepatocytes. These findings provide new insight into the functional changes in chronic obesity-induced type 2 diabetes and it is possible that the pathological feature make a contribution to promise the target of pharmacological therapy.

β-cryptoxanthin is a common carotenoid pigment found in fruit, especially in Satsuma mandarins and in persimmons. After ingestion, β-cryptoxanthin is distributed to and accumulates in organs, such as the liver, lung, and kidney. Recent studies have reported that because of its antioxidant defense, β-cryptoxanthin performs several important functions in the preservation of human health and in the prevention of several diseases, including cancer and osteoporosis. The present study aims to determine whether β-cryptoxanthin has a protective effect on renal glomeruli during acute nephritis. To develop our acute nephritis mouse model, we induced kidney inflammation in mice using lipopolysaccharide. To analyze pathological changes in the renal glomeruli of these mice, tissue sections of the kidney were analyzed by hematoxylin-eosin and periodic acid-Schiff staining. In mice with acute nephritis, we observed a thickening of the basal membrane in the renal glomeruli. By ultrastructural analysis, abnormalities in the foot cells were also identified. In the β-cryptoxanthin-ingested mice, these pathological changes were decreased. Migration of urinal proteins occurred in mice with acute nephritis, but this was decreased in β-cryptoxanthin-ingested mice, such that it correlated with the blood concentration of β-cryptoxanthin. Furthermore, in β-cryptoxanthin-ingested mice, both the accumulation and activation of inflammatory cells were decreased in the renal glomeruli. These results suggest that β-cryptoxanthin ingestion may produce great improvement in acute nephritis. These findings provide new insights into β-cryptoxanthin and its protective effect, and provide a new target for pharmacological therapy in human disease.

Chronic obesity is a known risk factor for metabolic syndrome. However, little is known about pathological changes in the small intestine associated with chronic obesity. This study investigated cellular and subcellular level changes in the small intestine of obese mice. In this study, a mouse model of obesity was established by early postnatal administration of monosodium glutamate. Changes in body weight were monitored, and pathological changes in the small intestine were evaluated using hematoxylin-eosin and Nissl staining and light and electron microscopy. Consequently, obese mice were significantly heavier compared with controls from 9 weeks of age. Villi in the small intestine of obese mice were elongated and thinned. There was reduced hematoxylin staining in the epithelium of the small intestine of obese mice. Electron microscopy revealed a significant decrease in and shortening of rough endoplasmic reticulum in epithelial cells of the small intestine of obese mice compared with normal mice. The decrease in rough endoplasmic reticulum in the small intestine epithelial cells of obese mice indicates that obesity starting in childhood influences various functions of the small intestine, such as protein synthesis, and could impair both the defense mechanism against invasion of pathogenic microbes and nutritional absorption.

Obesity, which is one of the causes of the lifestyle-related disease, is a hepatopathic exacerbation factor that causes a chronic hepatic disorder. In this study, we examined the pathological changes in the liver in mice with obesity induced by monosodium glutamate administration. Pathological analysis revealed the deposition of many lipid droplets in hepatocytes and sinusoidal dilatation in obese mice. Scanning electron microscopic analysis revealed the presence of sinusoidal dilatation, and the fenestrations of the sinusoid were significantly swollen in obese mice. These results suggest that a dysfunction of the sinusoidal endothelium occurs in chronic obesity.