A rare sugar, D-allulose (also called D-psicose), has recently been applied as a food supplement in view of controlling diabetes and obesity in Japan. D-allulose has been proven to have unique effects against hyperglycemia and hyperlipidemia in a number of studies using several species of rats and mice. However, the antiobesity effects of D-allulose have not yet been assessed in Lep(ob)/Lep(ob) (ob/ob) mice. Therefore, this study explored the dietary supplemental effects of this sugar in leptin-deficient ob/ob mice. Consequently, the subchronic ingestion of D-allulose in ob/ob mice for 15 wk significantly decreased the body and liver weights, and the loss of body weight was involved in the reduction of the total fat mass, including abdominal visceral fat, and not fat-free body mass, including muscle. Furthermore, D-allulose improved hepatic steatosis, as evaluated using hepatic histological studies and MRI. In the normal mice, none of these parameters were influenced by the single or long-term ingestion of D-allulose. These results indicate that dietary supplementation of D-allulose especially influences postprandial hyperglycemia and obesity-related hepatic steatosis, without exercise therapy or dietary restriction. Therefore, D-allulose may be useful as a supplement for preventing and improving obesity and obesity-related disorders.

Treatment of intracerebral hemorrhage is often pointless, although considerable effort has been devoted to developing treatments for ischemic stroke. The purpose of this study was to determine the influence of drugs in improving neurological outcomes with pharmaceutical therapy after intracerebral hemorrhage. The free-radical hypothesis for intracerebral hemorrhage is based on the cytotoxicity triggered by blood components and its degradation products, such as heme and iron as a potent pro-oxidant atom. Sulfaphenazole (SPZ) has a different mechanism such as reactive oxygen species scavenging, in addition to the inhibition of superoxide production by cytochrome P450. The present study investigated the properties of SPZ in collagenase-induced intracerebral hemorrhage rat brain damage. The results show that systemic SPZ treatment after intracerebral hemorrhage reduces striatal dysfunction, the elevation of lipid peroxidation, and brain edema in the rat. These results suggest that SPZ is a potentially effective therapeutic approach for intracerebral hemorrhage as the effect of SPZ was initiated for either 1 h or 3 d post-intracerebral hemorrhage.Key words intracerebral hemorrhage; magnetic resonance imaging; striatum; brain edema; rotation behavior; sulfaphenazole Intracerebral hemorrhage (ICH) results from the rupture of a blood vessel in the brain, and is a major public health problem, because ICH leads to a high rate of death and disability in adults. The 30-d mortality rate is approximately 50%, and most survivors (more than 80%) are left with neurological disabilities.1) Primary ICH accounts for approximately 25% of all strokes in Asian populations including the Japanese, 2) and spontaneous ICH represents one of the most devastating types of stroke.The pathophysiology of ICH is caused by a complex chain of events starting with disruption of the blood-brain barrier (BBB) and infiltration of blood components into the brain parenchyma, resulting in a progressive edema, which starts in the first 24 h and remains elevated over several days.3) The development of therapies relies on the use of animal models. 4)The animal models are commonly produced by manipulation in the striatum, because that is the most common site of ICH (more than 50% of all ICH).1) Rosenberg and coworkers have developed a particularly elegant rat model in which intrastriatal injection of bacterial collagenase (COL) disrupts the basal lamina of cerebral capillaries and causes bleeding into the brain tissue. 5) A highly reproducible brain injury due to ICH and the ability to follow changes in vivo are necessary to properly evaluate treatments.Oxidative stress is thought to be deeply involved in secondary brain injury after ICH.6) The amount of oxidative DNA is increased after ICH in the animal model, and administration of a free radical scavenger, edaravone suppressed DNA oxidation and brain damage after ICH.7) Iron plays a role in a proposed mechanism for the generation of oxidative stress after ICH.8) Iron ions are generated by hemoglobin breakd...

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