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Background: Many studies have shown that low copy number variation (CNV) of the salivary amylase gene (AMY1) and low serum amylase concentration are associated with impaired glucose metabolism and obesity. We aimed to clarify the conflicting results of previous studies by examining AMY1 expression and metabolic indices in a homogenous group of healthy participants.Methods: Sixty healthy non-obese young Japanese women aged 20 -39 years were examined for AMY1 CNV, salivary amylase, body mass index (BMI) and serum parameters including glycated hemoglobin (HbA1c), ketones, and total, salivary and pancreatic amylase. Respiratory quotient at rest and changes in blood glucose after starch loading were also examined.Results: AMY1 CNV (range, 4 -14) and the level of serum salivary amylase were correlated inversely with HbA1c (r = -0.36, P = 0.003 and r = -0.30, P = 0.02, respectively), whereas the percentage of serum salivary amylase in total serum amylase was positively correlated with blood glucose at 30 and 45 min after starch loading (r = 0.38, P = 0.004 and r = 0.27, P = 0.04, respectively). The level of serum total amylase, but not AMY1 CNV, was correlated inversely with BMI (r = -0.29, P = 0.02). Logistic regression analysis showed that low AMY1 CNV (4 -7) was significantly associated with an HbA1c of ≥ 5.4% (34 mmol/mol) even after adjustment for age, BMI and energy consumption, compared with high AMY1 CNV (8 -14).Conclusions: Although a higher percentage of serum salivary amylase was associated with higher levels of blood glucose at the early stage after starch loading, low AMY1 CNV was associated with chronic unfavorable glucose metabolism in healthy non-obese young women in Japan.

Nonalcoholic steatohepatitis (NASH) is characterized by excess lipid accumulation and inflammation inhepatocytes. In this study, to provide insight into the preventive effects of d-allose, a rare sugar, on the onset of NASH, we designed animal experiments using male STAM mice treated with streptozotocin and fed a high-fat diet (HFD). Experiments were initiated when the mice reached 5 weeks of age and lasted 3 weeks. After the 3-week protocol, mice fed the HFD containing d-allose exhibited significantly decreased serum alanine aminotransferase levels, hepatic lipid accumulation and inflammation, and improved nonalcoholic fatty liver disease activity score compared to mice fed HFD without d-allose ( p < 0.05). Further, hepatic mRNA expression of sterol regulatory element binding protein-1 (Srebp-1) and monocyte chemotactic protein-1 (Mcp-1) was lower in mice fed d-allose.These results suggested that d-allose prevented NASH by blocking hepatic lipid accumulation and progressive inflammation.Keywords: nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, rare sugar, d-allose IntroductionNonalcoholic fatty liver disease (NAFLD) is an increasingly common hepatic phenotype of metabolic syndrome not caused by chronic alcohol consumption and is characterized by lipid accumulation in hepatocytes (Williams et al., 2011). Nonalcoholic steatohepatitis (NASH), a type of NAFLD, is a significant risk factor for the development of cirrhosis and hepatocellular carcinoma (Feldstein et al., 2009;Cohen et al., 2011). The two-hit theory (Day and James, 1998) and multiple parallel hits hypothesis (Tilg et al., 2010) have been used to explain the progression of simple steatosis to NASH via lipid accumulation, inflammation, and oxidative stress in the liver, although the exact mechanisms R. Yamamoto et al. 320 have not yet been elucidated.In the alternative medicinal food sciences, recent reports have claimed that excessive sugar intake (e.g., d-fructose and highfructose corn syrup) is a high risk factor in the progression of NAFLD/NASH (Abdelmalek et al., 2010;Nseir et al., 2010).Meanwhile, the physiological effects of rare sugars, such as shown to protect against inflammatory and oxidative ischemia/ reperfusion (I/R) injury in liver, retinal, and cerebral injuries in rodent models (Hossain et al., 2003;Hirooka et al., 2006;Gao et al., 2013). Previous studies have revealed the physiological benefits Materials and MethodsAnimals and experimental design, and sample preparation STAM mice were used to model NASH and were obtained according to the method described by Fujii et al. (2013). Pathogenfree, 14-day pregnant female C57BL/6J mice were purchased from Charles River Laboratories (Tokyo, Japan). To induce NASH, STAM mice were primarily obtained by treating C57BL/6J mice with a single subcutaneous injection of 200 µg STZ (SigmaAldrich, St. Louis, MO, USA) 2 days after birth. At 4 weeks of age, the mice were fed a HFD (HFD32; CLEA Japan, Tokyo, Japan) ad libitum for 1 week (the experimental scheme is shown in Fig. 1). At 5 ...

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