We investigated the anti-obesity effects of D-psicose by increasing energy expenditure in rats pair-fed the high-sucrose diet (HSD). Wistar rats were divided into two dietary groups: HSD containing 5% cellulose (C) and 5% d-psicose (P). The C dietary group was further subdivided into two groups: rats fed the C diet ad libitum (C-AD) and pair-fed the C diet along with those in the P group (C-PF). Resting energy expenditure during darkness and lipoprotein lipase activity in the soleus muscle were significantly higher in the P group than in the C-PF group. Serum levels of glucose, leptin and adiponectin; glucose-6-phosphate dehydrogenase activities in the liver and perirenal adipose tissue; and body fat accumulation were all significantly lower in the P group than in the C-PF group. The anti-obesity effects of D-psicose could be induced not only by suppressing lipogenic enzyme activity but also by increasing EE in rats.

ta, and environmental factors. 1-3 Numerous extraintestinal manifestations occur in IBD, including lesions of the skin (erythema nodosum and pyoderma gangrenosum) 4 and of the joints (peripheral arthritis, sacroiliitis, and ankylosing spondylitis), 5,6 hepatobiliary complications (gallstones and primary sclerosing cholangitis), 7,8 and renal complications. 9 Immunoglobulin A nephropathy (IgAN) is one of the rare renal complications associated with IBD. 10-13 IgAN is one of the most predominant forms of glomerulonephritis, ultimately leading to end-stage renal failure in a high proportion of patients (approximately 30%-40%). 14 The International Kidney Biopsy Survey on glomerular disease frequencies, which consisted of 42,603 renal biopsies spanning 4 continents, diagnosed IgAN in 22.1% of all glomerular disease

Serum amyloid A (SAA) is an acute phase inflammatory protein that we previously described as a robust biomarker of colorectal inflammation in patients with ulcerative colitis (UC) in clinical remission. However, what induces SAA expression in UC remains unclear. This study demonstrates that SAA is significantly expressed in the intestinal tract of UC mouse models when compared with C-reactive protein, another inflammatory biomarker. Moreover, interleukin-6 and tumor necrosis factor-α were found to promote SAA1 expression, as were Toll-like receptor ligands flagellin and lipopolysaccharide. Furthermore, results suggested that the nuclear factor-kappa B (NF-κB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Therefore, the flagellin/NF-κB/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation.

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