Increased Apparent Diffusion Coefficient Values of Masticatory Muscles on Diffusion-Weighted Magnetic Resonance Imaging in Patients With Temporomandibular Joint Disorder and Unilateral Pain.

PURPOSE: Myalgia of the masticatory muscles is difficult to evaluate quantitatively. The purpose of the present study was to quantitatively assess myalgia of the masticatory muscles in patients with temporomandibular disorders (TMDs) using the apparent diffusion coefficient (ADC) on diffusion-weighted magnetic resonance imaging (MRI). PATIENTS AND METHODS: Patients who had undergone MRI with clinically diagnosed TMDs according to the criteria of the American Academy of Orofacial Pain and unilateral temporomandibular joint pain from March 2015 to January 2017 were prospectively enrolled. The MRI techniques used included axial diffusion-weighted imaging (DWI) and short T1 inversion recovery imaging through the neck to the skull base. The regions of interest were drawn to completely include the right and left lateral pterygoid muscles, medial pterygoid muscles, and masseter muscles on a slice demonstrating the largest area of each muscle on the ADC map. We compared each masticatory muscle of the pain side with those of the contralateral side without pain. RESULTS: A total of 106 patients with TMD had met the inclusion criteria (18 males, 88 females; mean age, 48.7 years; range, 16 to 80). The mean ADC values of the masticatory muscles of the pain side were significantly greater than those of the no-pain sides (P < .01), as were those for the lateral pterygoid muscles (1.35 ± 0.79 × 10-3 mm2/second vs 1.13 ± 0.77 × 10-3 mm2/second), medial pterygoid muscles (1.28 ± 0.46 × 10-3 mm2/second vs 1.05 ± 0.69 × 10-3 mm2/second), masseter muscles (1.33 ± 0.78 × 10-3 mm2/second vs 1.09 ± 0.64 × 10-3 mm2/second). CONCLUSIONS: The ADC values of the masticatory muscles on the pain side were significantly greater than those of the contralateral side without pain. Our results suggest that DWI could be used to assess myalgia of the masticatory muscles quantitatively.

Oral tributyrin prevents endotoxin-induced lipid metabolism disorder.

BACKGROUND & AIMS: Sepsis leads to dysregulation of lipid and lipoprotein metabolism. Butyrate increases peroxisome proliferator-activated receptors (PPARs), which are key nuclear hormone receptors to induce fatty acid oxidation and synthesis. Oral administration of tributyrin, a prodrug of butyrate contained in dairy products, suppresses lipopolysaccharide (LPS)-induced liver injury through attenuating nuclear factor-κB activity with an increased hepatoportal butyrate level. In this study, we elucidated the protective effect of oral administration of tributyrin against LPS-mediated lipid metabolism disorder in rats. METHODS: Male Wistar rats were randomly divided and were administered tributyrin or vehicle orally 1 h before LPS injection and then sacrificed at 0, 1.5, 6, and 24 h after LPS. Liver tissue expressions of nuclear hormone receptors, enzymes associated with fatty acid metabolism, and histone acetylation were analyzed by real-time polymerase chain reaction or western blotting. Plasma lipids levels were measured. RESULTS: Tributyrin enhanced expression of PPARs and histone H3 in the liver at basal levels. Tributyrin suppressed LPS-induced repression of PPARs fatty acid oxidation-associated enzymes: fatty acid transport protein and fatty acid binding protein, and fatty acid synthesis-associated enzyme: sterol regulatory element binding protein-1c. Tributyrin reduced the increase in plasma triglyceride, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels at 24 h after LPS injection. CONCLUSIONS: Oral tributyrin administration prevented elevation of plasma triglyceride, TC, and LDL-C levels through improved fatty acid oxidation in endotoxemic rats.

Mild obesity reduces survival and adiponectin sensitivity in endotoxemic rats.

BACKGROUND: Recent meta-analyses have reported that critically ill patients with morbid obesity (body mass index >40 kg/m(2)) have poor outcomes, but the effects and mechanisms of action of mild obesity are still unclear. The purpose of this study was to evaluate the effect of mild obesity using a lard-based, high-fat diet (HFD) on pathologic conditions and the mechanisms of adiponectin action in endotoxemic rats. MATERIALS AND METHODS: Male Wistar rats underwent HFD feeding for 4 wk and were killed at 0, 1.5, and 6 h after lipopolysaccharide (LPS) injection. Plasma levels of adiponectin, nitric oxide, and interleukin 6; messenger RNA expression of adiponectin receptors (AdipoR1 and AdipoR2) in the liver and the skeletal muscle; blood biochemical test results; and histology of the liver were analyzed. RESULTS: HFD-fed rats had a lower survival rate (12.8% versus 85.2%) and lower plasma adiponectin levels after LPS injection (P < 0.01). Messenger RNA expression of adiponectin receptors in the liver, but not the skeletal muscle, also decreased in HFD-fed rats (P < 0.05). Tissue injury and oxidative stress in the liver and plasma inflammatory mediator levels increased, and worsened lipid metabolism abnormalities were noted. The findings indicated that HFD decreased the sensitivity of adiponectin and was associated with an increase in oxidative stress and inflammation, which finally resulted in worsened liver injury and poor survival rate after LPS injection. CONCLUSIONS: Short-term, HFD-induced, mild obesity is harmful to the septic host, reduces adiponectin sensitivity, and could be the cause of worsening pathologic conditions.

Oral administration of tributyrin increases concentration of butyrate in the portal vein and prevents lipopolysaccharide-induced liver injury in rats.

BACKGROUND & AIMS: Short-chain fatty acids, especially butyrate, have various biological activities including inhibition of tumor necrosis factor (TNF)-α secretion, via attenuation of nuclear factor-κB (NF-κB) activation. Here, we evaluated the protective effect of oral administration of tributyrin, a prodrug of butyrate, on lipopolysaccharide (LPS)-induced liver injury in rats. METHODS: Rats were divided into four groups: normal control, tributyrin, LPS, and tributyrin/LPS (treated with tributyrin 1 h before LPS). Plasma levels of butyrate and TNF-α, expression of TNF-α, NF-κB, Toll-like receptor (TLR) 2, and TLR4 mRNA in liver, blood biochemical tests, and histopathological analysis of liver were performed. RESULTS: Oral tributyrin increased plasma butyrate level in the portal vein to 2.4 mM at 1 h and 0.7 mM at 2.5 h. Tributyrin attenuated NF-κB activation and liver tissue injury associated with LPS injection. The increases in TNF-α level, and hepatic TLR2 mRNA expression were lower in the tributyrin/LPS group. We believe that this study provides the first evidence that orally administered tributyrin increases butyrate level in the hepato-portal system and attenuates liver injury and subsequent inflammatory responses. CONCLUSION: Oral tributyrin increased plasma butyrate in the portal vein and attenuated liver injury in endotoxemic rats.