Measuring visceral fat with water-selective suppression methods (SPIR, SPAIR) in patients with metabolic syndrome.

We attempted to measure the area and volume of visceral fat using magnetic resonance (MR) imaging to avoid radiation exposure. We used water suppression-spectral attenuation with inversion recovery (WS-SPAIR) as prepulses and conducted T(1) high-resolution isotropic volume examination (THRIVE). Image processing software can be used to estimate the area and volume of fat and separate the fat and water signals at a visually optimal threshold in the MR image, which requires contrast enhancement between intestinal contents and visceral fat. In 14 volunteers, we evaluated WS-SPAIR and water suppression-spectral presaturation with inversion recovery (WS-SPIR) with respect to the relationship between the flip angle of THRIVE and signal contrast. We used flip angles of 5 degrees, 10 degrees, and 20 degrees. The minimum threshold that allowed exclusion of intestinal contents from the masked region was determined for each technique. The volume and area of the masked region, which included subcutaneous fat, were measured at the umbilicus level. Both volume and area increased with a smaller flip angle. The masked region was larger with WS-SPIR-THRIVE (flip angle 5 degrees ). The size of the masked region was determined according to the minimum threshold that allowed exclusion of the intestinal contents from the masked region, expressing the contrast between the intestinal contents and fat in a relative manner. It was speculated that by separating the signals at the threshold, WS-SPIR-THRIVE (flip angle 5 degrees) was a more suitable technique for measuring the area and volume of visceral fat.

MR measurement of visceral fat: assessment of metabolic syndrome.

One diagnostic criterion for metabolic syndrome is obesity from the accumulation of visceral fat; others include abdominal circumference and area of visceral fat as measured by computed tomography (CT) at the umbilical level. We evaluated visceral fat using frequency-selective excitation magnetic resonance (MR) imaging SPAIR (spectral attenuation with inversion recovery) water suppression THRIVE (3D T1-high resolution isotropic volume examination). Fifty of 70 slices with 2-mm interval were used to render and measure volume of visceral fat ranging within 10 cm of the umbilicus; the area of visceral fat at the umbilical level was also measured. Imaging was completed using breath hold within 14 s. Image processing was easier than using CT.

Herb medicine Inchin-ko-to (TJ-135) regulates PDGF-BB-dependent signaling pathways of hepatic stellate cells in primary culture and attenuates development of liver fibrosis induced by thioacetamide administration in rats.

BACKGROUND/AIMS: We studied the effect of Inchin-ko-to (TJ-135), a herb medicine that has been clinically used for liver cirrhosis in Japan, on liver fibrosis in a rat model and on the function of stellate cells. METHODS: Rat liver fibrosis was generated by thioacetamide (TAA) administration. DNA synthesis was assessed by 5-bromo-2'-deoxyuridine incorporation assay. Protein expression was analysed by western blotting. Collagen and fibronectin mRNA expression were analysed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: TJ-135 improved liver fibrosis induced in rats by TAA administration. TJ-135 reduced collagen deposition and the expression of smooth muscle alpha-actin in fibrotic liver tissues and decreased the serum level of hyaluronic acid. In primary-cultured stellate cells, TJ-135 suppressed DNA synthesis and the expression of collagen alpha 1(I), collagen III, and fibronectin mRNAs. It hampered DNA synthesis and migration of PDGF-BB-stimulated stellate cells through inhibiting phosphorylation of PDGF receptor-beta and down-stream signaling pathways. Among TJ-135 components, 3-methyl-1,6,8-trihydroxyanthraquinone (emodin) derived from Rhei rhizoma was found to be the most active molecule. CONCLUSIONS: TJ-135 and emodin regulate PDGF-dependent events in stellate cells and attenuate the development of liver fibrosis. Their clinical use may be beneficial for the therapy of human liver fibrosis.

Sulfur-containing amino acids attenuate the development of liver fibrosis in rats through down-regulation of stellate cell activation.

BACKGROUND/AIMS: We tested the pharmacological action of sulfur-containing amino acids on the development of liver fibrosis in rats and on the function of cultured stellate cells. METHODS: Liver fibrosis was induced in rats by thioacetamide administration or by ligating the common bile duct. DNA synthesis of cultured stellate cells was evaluated by BrdU incorporation. The expression of proteins and phospho-proteins was determined by western blot analysis. mRNA expression was evaluated by RT-PCR. RESULTS: Oral administration of l-cysteine or l-methionine attenuated the deposition of collagen in liver tissues in the two fibrotic models, accompanying a reduction in the expression of smooth muscle alpha-actin and platelet-derived growth factor receptor beta and mRNAs of collagens, transforming growth factor-betas and tissue inhibitors of matrix metalloproteinase. In cultured stellate cells, l-cysteine and l-methionine suppressed the DNA synthesis and the expression of growth factor receptors, smooth muscle alpha-actin and type I collagen. They hampered the phosphorylation of p44/42 MAPK and Akt under platelet-derived growth factor-BB stimulation. Stellate cells were found to express methionine adenosyltransferase 2A. CONCLUSIONS: l-Cysteine and l-methionine regulate the activation of stellate cells. Their oral supply aids the suppression of the progression of liver fibrosis.