Research Note: Expression of IGF-1 and IGF-1 receptor proteins in skeletal muscle fiber types in chickens with hepatic fibrosis.

We investigated the expression of insulin-like growth factor 1 (IGF-1) and IGF-1 type 1 receptor (IGF-1R) in skeletal muscle fiber types in chickens with hepatic fibrosis induced by bile duct ligation (BDL). Eleven hens, approximately 104 weeks old, were randomly assigned to BDL (n = 4) and sham surgery (SHAM; n = 7) groups. In BDL hens, histopathology revealed marked bile duct proliferation and liver fibrosis. The cross-sectional area (CSA) of myofibers from both the pectoralis (PCT) muscles significantly decreased in the BDL group compared with the SHAM group (P < 0.01). In contrast, the CSA of myofibers from the femorotibialis lateralis (FTL) muscle did not decrease in the BDL group. Type I fibers were large, round, and hypertrophic. Elongated type IIA and IIB fibers were also present. For IGF-1 immunostaining, the immunoreaction intensity was higher in the PCT in the BDL group than the SHAM group. Within the BDL group, type I fibers from FTL had a stronger immunoreaction intensity than the type II fibers. For IGF-1R immunostaining, the intensity of the immunoreactions was similar within the PCT in the BDL group compared with the SHAM group. For FTL, type I fibers had stronger reactions to IGF-1R than type II fibers in the BDL group. These results suggest that type I fibers express both IGF-1 and IGF-1R and become hypertrophic in chickens with hepatic fibrosis.

Bioactivities generated from meat proteins by enzymatic hydrolysis and the Maillard reaction.

Bioactive peptides are released from meat proteins by enzymatic hydrolysis (i.e., gastrointestinal digestion, aging/storage, fermentation, and protease treatment). Such peptides attribute physiological functions to meat and meat products and are promising food ingredients for developing functional foods. Meat by-products (e.g., blood and collagen) are also good sources for generating bioactive peptides, since they are produced in large quantities and are rich in proteins. Although protein-derived bioactive peptides are attractive ingredients, their changes by the Maillard reaction during processing, cooking, and storage should be investigated. This article briefly reviews the production of bioactive peptides from meat and meat by-products. Such diverse peptides affects circulatory, nervous, alimentary, and immune systems. Then, the bioactivities of Maillard reaction products (MRPs) generated from protein hydrolysates are discussed. Special attention is paid to bioactivities of 2,5-dimethyl-4-hydroxy-3(2H)-furanone (DMHF) inhalation. As such activities, we have evaluated the impact of DMHF on blood pressure, moods, brainwaves, and dietary intake. Our efforts for understanding various aspects and implication of peptides and MRPs from meat proteins would open new avenues in the meat and food industry.

DMHF (2,5-dimethyl-4-hydroxy-3(2H)-furanone), a volatile food component with attractive sensory properties, brings physiological functions through inhalation.

2,5-Dimethyl-4-hydroxy-3(2H)-furanone (DMHF) is an aroma compound found in various foods, and used widely in the flavor and perfume industry. Dilute DMHF solutions exhibit a strawberry-like flavor while DMHF concentrates have a caramel-like aroma. DMHF is an important flavor compound contributing to the sensory properties of various natural products and thermally processed foods. DMHF is generated by the Maillard reaction during cooking and processing and affects the palatability of foods. Although Maillard reaction products (e.g., melanoidins) have physiologically positive effects, effects of odors generated from by this reaction are relatively unknown. This chapter initially overviewed the Maillard reaction and the generation of volatile compounds. Then, properties of DMHF, which is an attractive volatile food component, is discussed. We focused particularly on bioactivities of DMHF inhalation in our previous studies.

Heart and brain circulation and CO2 in healthy men.

AIM: To compare blood flow response to arterial carbon dioxide tension change in the heart and brain of normal elderly men. METHODS: Thirteen healthy elderly male volunteers were studied. Hypercapnea was induced by carbon dioxide inhalation and hypocapnea was induced by hyperventilation. Myocardial blood flow [mL min(-1) x (100 g of perfusable tissue)(-1)] and cerebral blood flow [mL min(-1) x (100 g of perfusable tissue)(-1)] were measured simultaneously at rest, under carbon dioxide gas inhalation and hyperventilation using the combination of two positron emission tomography scanners. RESULTS: Arterial carbon dioxide tension increased significantly during carbon dioxide inhalation (43.1 +/- 2.7 mmHg, P < 0.05) and decreased significantly during hyperventilation (29.2 +/- 3.4 mmHg, P < 0.01) from baseline (40.2 +/- 2.4 mmHg). Myocardial blood flow increased significantly during hypercapnea (88.7 +/- 22.4, P < 0.01) from baseline (78.2 +/- 12.6), as did the cerebral blood flow (baseline: 39.8 +/- 5.3 vs. hypercapnea: 48.4 +/- 10.4, P < 0.05). During hypocapnea cerebral blood flow decreased significantly (27.0 +/- 6.3, P < 0.01) from baseline as did the myocardial blood flow (55.1 +/- 14.6, P < 0.01). However, normalized myocardial blood flow by cardiac workload [100 mL mmHg(-1) x (heart beat)(-1) x (gram of perfusable tissue)(-1)] was not changed from baseline (93.4 +/- 16.6) during hypercapnea (90.5 +/- 14.3) but decreased significantly from baseline during hypocapnea (64.5 +/- 18.3, P < 0.01). CONCLUSION: In normal elderly men, hypocapnea produces similar vasoconstriction both in the heart and brain. Mild hypercapnea increased cerebral blood flow but did not have an additional effect to dilate coronary arteries beyond the expected range in response to an increase in cardiac workload.

ABO-incompatible auxiliary partial orthotopic liver transplant for late-onset familial amyloid polyneuropathy.

A 60-year-old Japanese man with late-onset familial amyloid polyneuropathy type I (FAP transthyretin Met30) showed clinical improvement following auxiliary partial orthotopic liver transplantation (APOLT) from an ABO-incompatible living related donor. Preoperatively, plasmapheresis and immunosuppressant drugs were used to reduce serum antibodies against the donor's ABO type. APOLT was chosen so the residual liver could sustain the patient in the event of hyperacute rejection. OLT is applicable to late-onset FAP transthyretin Met30, and APOLT can be considered in ABO-incompatible cases.

Long-term effect of simvastatin on the improvement of impaired myocardial flow reserve in patients with familial hypercholesterolemia without gender variance.

BACKGROUND: Impaired myocardial flow reserve (MFR) in patients with familial hypercholesterolemia (FH) without evidence of ischemia has been reported. However, it has not been clarified whether diminished MFR in such male or female patients with FH can be reversed by simvastatin. METHODS AND RESULTS: Sixteen patients with FH and 16 age-matched control subjects were studied. All patients were proved to have no evidence of exercise stress-induced myocardial ischemia. Baseline myocardial blood flow (MBF) and MBF during dipyridamole administration (MBF [DP]) were measured with positron emission tomography and nitrogen 13 ammonia; MFR was then calculated before and 9 to 15 months after therapy with simvastatin (5-10 mg/day). Total cholesterol level was significantly higher in patients with FH (277 +/- 49.0) than in control subjects (190 +/- 14.9) but was normalized after lipid-lowering therapy (205 +/- 40.3). Baseline MBF was comparable among FH patients before (77.6 +/- 11.6 mL/min/100 g) and after therapy (74.5 +/- 9.62 mL/min/100 g) and control subjects (78.5 +/- 29.9 mL/min/100 g). However, MBF (DP) in FH patients before therapy (178 +/- 50.9 mL/min/100 g) was significantly lower than that in control subjects (282 +/- 148 mL/min/100 g) and was significantly improved after therapy (228 +/- 91.6 mL/min/100 g, P <.05). In fact, there was no statistically significant difference in the MBF (DP) value in FH patients after therapy compared with that in control subjects (P =.09). MFR significantly improved after therapy in patients with FH (3.33 +/- 1.19 vs 2.27 +/- 0.625, P <.01) and was then statistically comparable to that in control subjects (3.54 +/- 1.11). Improvement of MFR was observed whether MBF (DP) before therapy was greater than or less than 200 mL/min/100 g. MFR was improved in both male and female patients with FH. There was a significant relationship between percent change in plasma total cholesterol concentration and percent change in MFR before and after lipid-lowering therapy (r = -0.57, P <.05). CONCLUSIONS: Diminished MFR in patients with FH without evidence of ischemia can be reversed by moderate- to long-term simvastatin therapy without gender variance.

Troglitazone improves whole-body insulin resistance and skeletal muscle glucose use in type II diabetic patients.

UNLABELLED: Recently, troglitazone has emerged as an insulin sensitizer for the treatment of type II diabetes. However, its effect on skeletal muscle glucose use (SMGU) has not been studied. METHODS: To investigate the effect of troglitazone on SMGU in patients with type II diabetes, we undertook skeletal muscle (18)F-FDG PET dynamic imaging under insulin clamping before and after administration of SMGU to 20 patients with type II diabetes. Data were compared with those for 12 age-matched healthy volunteers. RESULTS: The whole-body glucose disposal rate (GDR) was significantly lower in patients (29.9 +/- 9.83 micromol/min/kg) than in control subjects (55.6 +/- 16.5 micromol/min/kg, P < 0.01), as was the SMGU (patients, 3.27 +/- 2.17 micromol/min/kg; control subjects, 10.9 +/- 6.4 micromol/min/kg; P < 0.01). After the therapy, GDR significantly improved in patients (29.3 +/- 14.6 micromol/min/kg, P < 0.05), as did SMGU (5.06 +/- 2.11 micromol/min/kg, P < 0.05). When results for patients with and without hypertension were separately analyzed, a significant improvement in SMGU after troglitazone was seen in both normotensive and hypertensive patients (normotensive [n = 10]: baseline, 3.67 +/- 2.89 micromol/min/kg; after therapy, 5.28 +/- 2.61 micromol/min/kg; P < 0.05; hypertensive [n = 10]: baseline, 2.89 +/- 1.22 micromol/min/kg; after therapy, 4.72 +/- 1.39 micromol/min/kg; P < 0.05). GDR in patients with and without hypertension was significantly improved by troglitazone (normotensive: baseline, 17.9 +/- 10.2 micromol/min/kg; after therapy, 31.9 +/- 15.9 micromol/min/kg; P < 0.01; hypertensive: baseline, 39.6 +/- 15.1 micromol/min/kg; after therapy, 47.7 +/- 23.8 micromol/min/kg; P < 0.05). The plasma free fatty acid concentration during insulin clamping was not changed by troglitazone (baseline, 1.1 +/- 0.86 mEq/L; after therapy, 0.93 +/- 0.65 mEq/L; P = not significant). CONCLUSION: Troglitazone can improve whole-body insulin resistance through the improvement of SMGU but not through a decline in plasma free fatty acid concentration in patients with type II diabetes with or without hypertension.

Metabolism of 99mTc-ethylcysteinate dimer in infarcted brain tissue of rats.

UNLABELLED: Brain SPECT with 99mTc-ethylcysteinate dimer (99mTc-ECD) reveals a subacute cerebral infarct as a hypoactive area, even in the presence of postischemic hyperperfusion. The brain retention of 99mTc-ECD depends on hydrophilic conversion mediated by enzymes, and impaired enzymatic trapping is hypothesized to depress the retention efficiency in the infarcted region. The aim of this study was to determine whether the metabolic rate of 99mTc-ECD is actually reduced in infarcted brain tissue. METHODS: In 50 mmol/L phosphate buffer (pH 7.4), 99mTc-ECD was incubated for 30 min with homogenates of rat brain tissue with and without triphenyltetrazolium chloride (TTC) staining. The ratio of polar products was determined by thin-layer chromatography as a function of incubation time, and metabolic rates were obtained. Permanent focal ischemia was induced by occlusion of the right middle cerebral artery (MCA) in rats. The brain was removed 24 h after MCA occlusion, and the infarcted area was defined by TTC staining. The metabolic rate of 99mTc-ECD was determined in homogenates of infarcted tissue, contralateral noninfarcted tissue, and tissue sampled from sham-operated rats. The infarct volume was measured by direct and indirect methods to assess volume expansion caused by edema, and the metabolic rate in infarcted tissue was corrected for the effect of edema. RESULTS: TTC staining had no effect on the metabolic rate of 99mTc-ECD. The metabolic rates in the infarcted tissue were 0.222%/min +/- 0.054%/min and 0.285%/min +/- 0.064%/min before and after correction for edema, respectively. These rates were significantly lower than those in the contralateral noninfarcted tissue (0.426%/min +/- 0.028%/min) and the tissue sampled from the sham-operated rats (0.439%/min +/- 0.031%/min). No substantial difference in rates was observed between the contralateral tissue and the tissue from the sham-operated rats. CONCLUSION: The results of this study showed that infarction decreases the activity of enzymes that mediate the hydrophilic conversion of 99mTc-ECD in the brain and suggest that reduced metabolic activity is related to decreased accumulation of 99mTc-ECD in hyperperfused infarcts.

Estimation of 99mTc-MAG3 clearance by single-sample methods and camera-based methods.

We compared single-sample methods, proposed by Russell et al. and Bubeck et al., and camera-based methods in calculating 99mTc-MAG3 clearance, and determined camera-based methods that provide estimates comparable to those measured by the Russell method. Twenty-one patients underwent 99mTc-MAG3 renal scintigraphy, and clearance was measured by the Russell method and Bubeck method. Various renogram parameters were determined based on the slope of the renogram and area under the renogram, and correlated with the clearance measured by the Russell method. Camera-based clearance was calculated with the obtained regression equations and with equations determined previously using the Bubeck method as a standard. The Bubeck method provided lower measures than the Russell method in high renal function. Clearance measured by the Russell method was well correlated with renogram parameters, and clearance calculated with the obtained regression equation was comparable to that measured by the Russell method. When camera-based clearance was predicted with the previous equation, it was lower than the result obtained by the Russell method in high function. In conclusion, there are systematic differences in 99mTc-MAG3 clearance calculated by different methods. The camera-based methods obtained in this study appear to facilitate comparison of results obtained by the Russell method and camera-based method.