Effects of 830 nm low-power laser irradiation on body weight gain and inflammatory cytokines in experimental diabetes in different animal models.

BACKGROUND AND AIMS: The present investigation was carried out to determine the levels of blood serum components and inflammatory cytokines in diabetic rat models [Goto-Kakizaki (GK), Zucker, and streptozotocin (STZ)-induced Sprague Dawley (SD) rats] which underwent abdominal Low-Power Laser Irradiation (LPLI) and compare them with non-irradiated controls. METHODS: The animals were subdivided into the following groups: diabetic control rats (GK, Zucker, STZ) and diabetic rats treated with LPLI (GK + LPLI, Zucker + LPLI, and STZ + LPLI) (n = 7). The animals were irradiated three times weekly for 12 weeks in LPLI (830 nm) at a dose of 5 J/cm2 for 500 s. RESULTS: Body weight was significantly lowered in the Zucker- LPLI group compared to control at 10 weeks and this pattern was maintained until 12 weeks of age. TNF-α, IL-1I and IL-6 levels were significantly decreased (5.1 ± 1.1 vs 3.3 ± 0.5, p < 0.01; 43.6 ± 8.8 vs 27.1 ± 3.8, p < 0.01; 98.3 ± 15.8 vs 62.2 ± 12.1, p < 0.01) in the Zucker- LPLI group compared with the control rats. The small intestinal transit rates of charcoal meals were significantly decreased (58.1 ± 10.1 vs 73.4 ± 13.3, p < 0.05) in the Zucker-LPLI group compared with the control rats. Similarly, the serum levels of glucose, cholesterol and triglycerides of LPLI groups were decreased in comparison with that of diabetic control rats. CONCLUSIONS: We suggest that abdominal LPLI can reduce body weight and LPLI could be applicable for use against diabetic-induced inflammatory factors.

Subjective global assessment is not sufficient to screen patients with defective hepatic metabolism.

BACKGROUND AND AIMS: Subjective global assessment (SGA) is useful for screening malnourished patients with several diseases, although it has been indicated to underestimate nutritional status for patients with liver disease. Accordingly, the aim of this study was to examine the usefulness of SGA as a nutritional screening tool for patients with liver disease, compared to patients with gastroenterological disease, without bias of personal ability and experience. METHODS: SGA was performed on 129 of hospitalized patients (86 with liver disease and 43 with gastroenterological disease). Nutritional status was categorized as well-nourished or malnourished status, based on nutritional indicators from laboratory data. RESULTS: The SGA screening ratio (sensitivity) for malnourished patients with liver disease was significantly lower than gastroenterological disease, while specificity or efficiency was not significantly different. In nutritional indicators from laboratory data, the difference between SGA-positive and SGA-negative patients with liver disease was significant but not so remarkable compared with the difference between those with other diseases. The positive number of SGA components per patient for the liver disease group was significantly less than gastroenterological disease group. CONCLUSIONS: SGA for patients with liver diseases was not sufficient as a nutritional screening tool because malnutrition induced by defective hepatic metabolism was not characterized fully.

Branched-chain amino acid supplements reduced ascites and increased the quality of life in a patient with liver cirrhosis: A case report.

Liver cirrhosis is frequently accompanied by malnutrition and hypoalbuminemia, which in turn commonly induces ascites in patients with liver cirrhosis. Ascites leads to abdominal distention and appetite loss, resulting in a deteriorated quality of life (QOL). Administration of branched-chain amino acid (BCAA)-rich supplements reduces hepatic encephalopathy and malnutrition. In addition, BCAAs by themselves up-regulate albumin synthesis through an increase in Fisher's ratio. Thus, in patients with liver cirrhosis, BCAA-rich supplements seem to be effective at reducing ascites and improving the QOL. Here, we report the case of a 58-year-old Japanese man with liver cirrhosis with severe ascites and peripheral edema. The hepatic function of the patient was classified as Child-Pugh grade C. To reduce protein-energy malnutrition, BCAA-rich supplements were administered as a late evening snack as part of a regimen including 2000 kcal/day (32.5 kcal/kg/day) of total energy and 83.5 g/day (1.3 g/kg/day) of total protein intake. Eight weeks after admission, ascites and edema had decreased. Nutritional status also improved from the time of admission to discharge; the serum BCAA level increased from 365.4 to 450.2 µmol/l. Furthermore, the ratio of BCAAs to tyrosine (BTR) increased from 1.70 to 3.65. We also evaluated the effects of nutritional therapy on the patient's QOL using the Medical Outcomes Study 36-Item Short-Form Health Survey upon admission and at discharge. All subscores showed marked improvement and reached a level greater than the Japanese norm with nutritional treatment. In conclusion, BCAA supplementation not only reduced ascites, but also improved the QOL in a patient with liver cirrhosis.

Expression of cystatin C prevents oxidative stress-induced death in PC12 cells.

Cystatin C, an inhibitor of cysteine proteinases, is suggested to be involved in oxidative stress-induced apoptosis of cultured CNS neurons and various neuronal diseases in vivo; however, little is known about its mechanism of action. To address the role cystatin C plays in oxidative stress-induced neuronal cell death, we established PC12 cell lines that stably expressed rat cystatin C. These cystatin C-expressing PC12 cells showed remarkable resistance to high (50%) oxygen atmosphere. This resistance correlate with expression levels of cystatin C, demonstrating that cystatin C has a protective effect on high oxygen-induced cell death. In contrast, in a normal (20%) oxygen atmosphere neither control nor cystatin C-expressing PC12 cells showed a significant change in the number of living cells, indicating that cystatin C does not play an important role in the regulation of cellular proliferation. Furthermore, the cystatin C-expressing cell line also resisted other oxidative stresses, including glutamate- and 13-L-hydroperoxylinoleic acid (LOOH)-induced cell death. These results demonstrate that cystatin C has protective effects against various oxidative stresses that induce cell death.