Nihon Naibunpi Gakkai zasshi最新文献

It has been reported recently that A2 allele of muscle glycogen synthase gene determined by Xba I RFLP (restriction fragment length polymorphism) is related to the frequency of NIDDM in Finland. Using PCR-RFLP analysis, we detected no A2 allele in Japanese patients with NIDDM and control. We found a new microsatellite of CA repeat in the human muscle glycogen synthase gene, and the polymorphism of the repeat number was detected by the polymerase chain reaction. Six different alleles were observed, indicating the highly polymorphic nature of this marker. We analyzed the repeat numbers and the genotypes in diabetics and control. The allele frequencies were not significantly different between NIDDM and control. However, the allele frequencies in the patients without high total cholesterolemia was significantly different from those of control. These findings suggest that the muscle glycogen synthase gene or neighboring genes are related to one of the disease genes of diabetes mellitus without high total cholesterolemia.

On the basis of a biochemical study of thyroid papillary and follicular carcinoma tissue (original focus, its periphery and cervical lymph node metastasis), we endeavoured to determine whether or not there was any Tg in the metastatic lymph node, and if there was, to extract and refine it, and also to determine the biochemical properties of Tg. We also investigated the relationship between the increase of blood Tg and the status of lymph node metastasis after surgery for thyroid carcinoma. There was found to be a noticeable decrease in Tg content per unit weight of the metastatic lymph node, and the iodine content in most cases had dropped almost to zero. This means that although Tg is biosynthesized in the metastatic lymph node, there is, in most cases, less than one atom of iodine per molecule of Tg, and we could find very little evidence of the formation of the thyroid hormone. As far as avidity for the antibody is concerned, that in cancer tissue Tg was much lower than that in healthy tissue Tg, and this was even more noticeable in metastatic node Tg than in primary focus Tg. In the sugar chain structure of the metastatic node, there was a lack of uniformity not seen in healthy tissue. In the lymph node metastatic focus, the production of structural Tg was noted. We also recognized the possibility that the increase of blood Tg level following surgery originates from the metastatic lymph nodes and other sites of recurrence.

Obesity is considered to be one of the major risk factors for developing non-insulin dependent diabetes mellitus (NIDDM). Our cohort study for NIDDM in Aito, Shiga 1980-1990 confirmed that aging, higher body mass index (obesity) and high blood pressure were independent risk factors for developing NIDDM in Japan. In Pima Indians, decreased glucose disposal rate (GDR) is significantly related to percentage of body fat (%fat). Insulin signaling for glycogen synthesis in the skeletal muscles is impaired in the early stages of obesity. Although the molecular mechanism for insulin resistance in obesity is still unknown, hyperinsulinemia induces insulin receptor loss by means of the down regulation mechanism, and prolonged hyperglycemia may induce the impairment of insulin receptor kinase in the skeletal muscles in obese subjects. These dysfunctions in insulin signaling may cause the deterioration of insulin sensitivity, resulting in worsening glycemic control. Thus dysfunction of insulin receptor signaling in skeletal muscles may be a target for preventing diabetes in obese subjects.

The present study was undertaken to clarify the effects of insulin and glucose on the utilization of non-esterified fatty acid (NEFA) in the resting rat skeletal muscle using the perfusion technique. The 24hr-starved and non-starved rat hind limbs were perfused for one hour with the perfusion mediums containing 1mM palmitate and various concentrations of glucose and insulin, and sampling was performed to calculate the clearance of NEFA (F value). In the absence of glucose, the F value of the starved rat hind limb was less than that of the non-starved rats, independently of insulin concentrations (0 and 125 microU/ml) in the perfusion medium (p < 0.02). Moreover, there was no influence of insulin on the F value in both the starved and the non-starved groups. In the presence of 13.9mM glucose, there were no statistically significant differences in the F value without insulin between the non-starved and starved groups. However, the F value was increased in the presence of 62.5 or 125 microU/ml insulin, compared with that in the absence of insulin (p < 0.001), although when the insulin concentration was elevated to 500 microU/ml, it was decreased. Both in the non-starved and the starved groups independently of insulin concentrations, the F value in the glucose-added condition was increased, compared with that in the absence of glucose. These results indicated that the utilization of NEFA in the resting rat skeletal muscle was facilitated by the moderate supply of glucose, although it was suppressed by the presence of abundant glucose.

A 57-year-old man was admitted to our hospital because of dyspnea due to congestive heart failure caused by hypertensive heart disease in September, 1992. Twenty years ago, he was diagnosed to be hypertensive, and in 1980, he was diagnosed to at our hospital to have primary aldosteronism (PA) due to a right aldosterone-producing adrenocortical adenoma (APA). There were no hypertensive vascular complications at that time. He refused surgical removal, and anti-hypertensive drugs including spironolactone were administered. However, his drug compliance was very inaccurate. On this recent admission, left ventricular hypertrophy associated with impaired contractivity, hypertensive retinal change and mild protein uria were noted, but no hematuria was detected. His renal function was impaired (Ccr: 15.2ml/min). An abdominal CT scan showed a typical right APA, bilateral renal atrophy and fine granular calcification at renal medulla, even though he had no hypercalcemia and hypercalciuria. In addition, multiple cerebral infarction was demonstrated by a brain CT scan, along with coronary artery stenoses at the right coronary artery and left circumflex branch by coronary angiography and bilateral multiple renal artery stenoses by renal angiography. Right adrenalectomy and renal biopsy were performed. Histological examinations revealed a yellow tan-colored APA, many sclerotic glomerulus, and severely hyarinized renal arterioles. After adrenalectomy, blood pressure was not normalized but was controlled easily by hypotensive agents. Impaired renal function was not improved and deteriorated slightly but did not get worse there after. Since 1959, including ours, 22 cases of APAs complicated with chronic renal failure were reported in Japan. In conclusion, surgical removal should be recommended for APA, even if the patient's condition is complicated with chronic renal failure.

A rare case of a patient with non-insulin-dependent diabetes mellitus (NIDDM) with small cell lung cancer, initially diagnosed as pyogenic vertebral osteomyelitis, was reported. A 40-year-old male patient was diagnosed with NIDDM about 3 years earlier, but he did not receive any treatment. Then, a two-month history of high fever, persistent cough and back pain developed. Chest X-ray film showed a lung infiltrate with a small cavity in the upper portion of the left lung. Computed tomography and magnetic resonance imaging of the chest revealed a tumor mass shadow with osteoclasia along the bodies of the 6th and 7th thoracic vertebral bone. Staphylococcus aureus infection was confirmed by arterial blood culture. Administration of antibiotics resulted in the disappearance of the left lung infiltrate and a slight reduction of the tumor mass in the thoracic vertebral bone, suggesting pyogenic vertebral osteomyelitis as an unusual complication of NIDDM. However, as the tumor mass still remained, needle biopsy for the mass lesion was performed, resulting in the diagnosis of metastasis of small cell carcinoma from the left lung. Gene aberration in this lung disease has been reported recently, and its correlation with NIDDM which may also be induced by genetic abnormality is an interesting question that remains to be resolved.

An unconscious woman of short stature (141 cm) was admitted to our hospital in March, 1994. She had hyponatremia (120 mEq/l) and had experienced massive bleeding during delivery. No increment of either plasma ACTH or cortisol levels was observed after insulin-induced hypoglycemia. However, urinary 17OHCS levels gradually increased after repeated intramuscular injections of ACTH. Plasma free T3 and free T4 levels were low. Neither plasma TSH nor prolactin (PRL) levels increased after an intravenous injection of TRH. Basal plasma LH, FSH and growth hormone (GH) levels were low and there were no observable responses to any of the stimulation tests. A magnetic resonance image (MRI) of her pituitary gland showed an empty sella. These results showed that she had a panhypopituitarism with primary empty sella. Replacement therapy with glucocorticoid was started and serum sodium levels normalized immediately. Levothyroxine was also administered. The possibility of pituitary dwarfism during her youth and a gradual postpartum reduction of other pituitary hormones may have caused an impairment of the hypothalamo-pituitary-adrenal axis.

This study evaluated phosphate excretion in response to atrial natriuretic peptide during acute hypocapnia in the presence or absence of the renal nerves in rats. To achieve a hypocapnic state, rats were mechanically hyperventilated with room air. As mechanical ventilation per se has been reported to affect renal excretory functions depending on the ventilatory conditions, this study was designed to examine renal functions during acute hypocapnia as compared with those during normocapnia produced by normal and/or hyperventilation. Rats were divided into three experimental groups: 1) a normally ventilated normocapnic (control) group (n = 8), 2) a hyperventilated normocapnic group (n = 8), and 3) a hyperventilated hypocapnic group (n = 8). The innervated right kidney served as a control for the contralateral denervated kidney. Acute renal denervation produced a greater phosphaturia compared to the innervated kidney during the control period in the two normocanic groups but not in the hypocapnic group. Infusion of ANP 12 micrograms/kg/h produced a remarkable increase in phosphate excretion in either kidney in the normocapnic groups. The degree of the phosphaturia (delta FEPi%) during infusion of ANP was similar between the normally ventilated and hyperventilated normocapnic groups both in innervated (10.6 +/- 2.4% and 7.4 +/- 1.2%) and denervated (14.0 +/- 3.0% and 13.5 +/- 2.2%) kidneys. In contrast to both normocapnic groups, the hypocapnic group had a greater hypophosphaturia during the control and ANP infusion periods in either kidney. The increase in fractional excretion of phosphate was smaller both in innervated (0.34 +/- 0.34% delta FEPi) and denervated (0.72 +/- 0.69% delta FEPi) kidneys than that in the other two normocapnic groups.(ABSTRACT TRUNCATED AT 250 WORDS)