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Biomedical subjects

Tomoatsu Nakamura

Publications and source records attributed to Tomoatsu Nakamura.

7 recordsLinked to original sources
PubMed2003

Relationship between exercise training-induced increase in insulin sensitivity and adiponectinemia in healthy men.

Circulating concentrations of adiponectin, an adipocyte-derived protein, are increased by thiazolidinediones and by weight reduction, accompanied with improvement in insulin sensitivity. The effect of exercise training, another therapy to increase insulin sensitivity (SI), on adiponectinemia is currently unclear. The present study was undertaken to clarify whether exercise training-induced increase in SI is related to changes in adiponectinemia in healthy men. Twelve healthy non-obese men underwent ergometer training at lactate threshold (LT) intensity for 60 min/day for 5 days/week for 6 weeks. An insulin-modified intravenous glucose tolerance test was performed before and at 16 h and 1 week after the last training session to determine SI using a minimal-model approach. Serum levels of adiponectin were determined at the same time. After the exercise training, VO2max and LT were significantly increased by 7.2% and 22.3% (P<0.01), while BMI and body fat mass remained unchanged. SI was significantly increased at 16 h after the last training session (from 7.0 +/- 3.1 to 9.6 +/- 3.6 [x 10(-4) x (microU/ml)(-1) x min(-1)], P<0.01), but returned toward the basal levels at 1 week after the cessation of the training. Serum adiponectin concentrations before the training (20.9 +/- 7.4 microg/ml) were positively correlated with SI. The concentrations were slightly but significantly decreased at 16 h (17.2 +/- 6.6 microg/ml, P<0.05), and returned to the basal values at 1 week after the training. From these results, it can be concluded that exercise training-induced increase in SI is not dependent on the increase in adiponectinemia in healthy men.

Adiponectin↗
PubMed2003

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency.

OBJECTIVE: Hyponatremia occurs not infrequently in hypopituitarism. Arginine vasopressin (AVP)-induced impaired water excretion is found in patients with hypopituitarism and experimental models of glucocorticoid deficiency. DESIGN: The present study was undertaken to determine whether augmented release of AVP is involved in the development of hyponatremia in elderly subjects with secondary adrenal insufficiency. METHODS: Forty patients with ACTH-deficient, secondary adrenal insufficiency were examined. They were divided into three groups according to the age at which diagnosis was ascertained (group A <20 Years, group B 20-64 Years, and group C>or=65 Years). RESULTS: Hyponatremia was more manifest in the elderly group than in the other two groups, serum sodium (Na) levels being 124.7 mmol/l in the elderly group, a value significantly less than 141.5 and 133.5 mmol/l in groups A and B. Plasma AVP levels seemed likely to be high compared with the respective hypo-osmolality in plasma in the elderly group, as plasma AVP levels were 1.7 pmol/l despite a mean plasma osmolality of 259 mmol/kg. Such an alteration was less clear in group B and was not found in group A. Therefore, elevation of plasma AVP was apparent in the elderly patients. Hydrocortisone replacement promptly normalized serum Na levels from 125 to 142 mmol/l (P<0.01) and reduced plasma AVP levels from 1.7 to 0.9 pmol/l (P<0.05), which were comparable to the respective plasma osmolality in the elderly patients. CONCLUSION: These results indicate that non-suppressible release of AVP is crucially involved in the impaired water excretion and hyponatremia seen in elderly patients with secondary adrenal insufficiency compared with the younger patients, and that exaggerated release of AVP becomes manifest as the subjects grow older.

Adolescent↗
PubMed2002

S(G), S(I), and EGP of exercise-trained middle-aged men estimated by a two-compartment labeled minimal model.

To examine the effects of physical training on glucose effectiveness (S(G)), insulin sensitivity (S(I)), and endogenous glucose production (EGP) in middle-aged men, stable-labeled frequently sampled intravenous glucose tolerance tests (FSIGTT) were performed on 11 exercise-trained middle-aged men and 12 age-matched sedentary men. The time course of EGP during the FSIGTT was estimated by nonparametric stochastic deconvolution. Glucose uptake-specific indexes of glucose effectiveness (S(2*)(G) x 10(2): 0.81 +/- 0.08 vs. 0.60 +/- 0.05 dl. min(-1). kg(-1), P < 0.05) and insulin sensitivity [S(2*)(I) x 10(4): 24.59 +/- 2.98 vs. 11.89 +/- 2.36 dl. min(-1). (microU/ml)(-1). kg(-1), P < 0.01], which were analyzed using the two-compartment minimal model, were significantly greater in the trained group than in the sedentary group. Plasma clearance rate (PCR) of glucose was consistently greater in the trained men than in sedentary men throughout FSIGTT. Compared with sedentary controls, EGP of trained middle-aged men was higher before glucose load. The EGP of the two groups was similarly suppressed by approximately 70% within 10 min, followed by an additional suppression after insulin infusion. EGP returned to basal level at approximately 60 min in the trained men and at 100 min in the controls, followed by its overshoot, which was significantly greater in the trained men than in the controls. In addition, basal EGP was positively correlated with S(2*)(G) . The higher basal EGP and greater EGP overshoot in trained middle-aged men appear to compensate for the increased insulin-independent (S(2*)(G)) and -dependent (S(2*)(I)) glucose uptake to maintain glucose homeostasis.

Adult↗
PubMed2002

Urinary excretion of aquaporin-2 water channel in diabetic ketoacidosis.

We studied the changes in plasma arginine vasopressin (AVP) and urinary excretion of aquaporin-2 (UAQP-2) water channel in 3 patients with diabetic ketoacidosis. They had marked hyperglycemia of 27.9 +/- 2.8 mmol/l (mean +/- SEM), and elevated hemoglobin A1c of 8.8 +/- 1.4%. Circulatory blood volume was decreased by approximately 25%, which was determined by the changes in hematocrit. Plasma AVP levels were elevated to 10.3 +/- 3.0 pmol/l and UAQP-2, 578 +/- 200 fmol/mg creatinine (normal, 153 +/- 28) at the hospitalization. When hyperglycemia was improved by the intravenous infusion of a small dose of insulin plus fluid administration, both plasma AVP and UAQP-2 promptly decreased to 1.2 +/- 0.2 pmol/l and 252 +/- 29 fmol/mg creatinine on day 7, respectively. These alterations were concomitant with the recovery of circulatory blood volume. In the present study, UAQP-2, in addition to plasma AVP, indicates circulatory blood volume depletion, and the changes in UAQP-2 estimates the AVP-dependent recovery of circulatory blood volume during the therapeutic period in the patients with diabetic ketoacidosis.

Adult↗
PubMed2002

Decrease in urinary excretion of aquaporin-2 associated with impaired urinary concentrating ability in diabetic nephropathy.

Aquaporin-2 (AQP-2) is known to be expressed in the renal collecting duct cells and participates in urinary concentration in response to arginine vasopressin (AVP). The present study was undertaken to determine whether progression of renal dysfunction affects urinary excretion of AQP-2 in diabetic nephropathy. The study was composed of 8 control subjects and 14 patients with type 2 diabetes classified into two groups according to serum creatinine level (cut-off point; 1.5 mg/dl). After an 8-hour water deprivation, both urinary osmolality (U(osm)) and urinary excretion of AQP-2 significantly decreased in the diabetic patients with chronic renal failure as compared to the control subjects (p < 0.0001, p < 0.05, respectively). After a water load (10 ml/kg), no differences were found in plasma osmolality (P(osm)), AVP levels and U(osm), whereas urinary excretion of AQP-2 significantly decreased in the patients with chronic renal failure as compared to the control subjects (p < 0.05). These results indicate that the decreased urinary excretion of AQP-2 in diabetic nephropathy is due to the impaired cellular signaling of AVP in collecting duct cells, which may be partly involved in the urinary concentrating defect in renal failure.

Aquaporin 2↗