Bone resorption and cortical bone striations occur in untreated patients with Graves' thyrotoxicosis. The bone resorption rapidly ameliorates after normalization of thyroid hormone levels. In contrast, the accelerated bone formation persists for at least 4-8 months, suggesting positive uncoupling of bone remodelling. This dominant bone formation could result in the improvement in cortical bone striations and the increase in bone mineral density of trabecular bone.

Objective We evaluated the relationship between glycated hemoglobin (HbA 1c ) in diabetic patients with stable glycemic control and the average fasting blood glucose (FBG) and postprandial blood glucose (PPG) values of 4 weeks prior to HbA 1c measurement and compared the results with glycated albumin (GA). Research design and methods Fifty-one diabetic patients were asked to use self-monitoring blood glucose to measure FBG before breakfast and PPG 1 and 2 h after breakfast 1 day a week for 4 weeks while maintaining normal daily activities. During monthly outpatient visits, HbA 1c and GA were measured. Data were analyzed in 40 patients, with \1% variation in HbA 1c values over 4 months. Results HbA 1c was best predicted by the average FBG (AvFBG) and the average of 1-h and 2-h PPG (AvMPPG) (adjusted R 2 = 0.51; HbA 1c = 4.35 ? 0.013 AvFBG ? 0.0056 AvMPPG). The contribution ratio was 0.013:0.0056, showing about 2.3 times greater contribution by FBG. GA was best predicted by the AvFBG and the average of 2-h PPG (Av2hPPG) (adjusted R 2 = 0.55; GA = 9.36 ? 0.0241 AvFBG ? 0.0430 Av2hPPG). The contribution ratio was 0.024:0.043, showing about 1.8 times greater contribution by 2-h PPG. This converse contribution of fasting and postprandial glucose to HbA 1c and GA was more prominent in insulin-treated patients than in untreated patients. Conclusions HbA 1c and GA can be satisfactorily predicted by FBG and PPG. HbA 1c reflects FBG more so than PPG, whereas GA better reflects PPG. Thus, depending on the characteristics of the glycated protein, a different glycemic status is reflected.

Abstract. The present study was undertaken to determine the pathophysiological role of arginine vasopressin (AVP) in elderly patients with hyponatremia, and the efficacy of fludrocortisone acetate in treating their hyponatremia. Eleven hospitalized patients aged 65 years or older whose serum sodium levels were less than 130 mEq/l were examined. The hyponatremic patients included two groups of patients: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and central salt-wasting syndrome. And 24 healthy, young subjects aged 20 to 34 years, and 24 healthy, elderly subjects aged 65 to 80 years were recruited by community announcement. The elderly subjects had decreased urinary concentrating ability and exaggerated response of AVP secretion to osmotic and nonosmotic stimuli, as compared to the young subjects. All the patients had hyponatremia, with the exaggerated urinary loss of Na. Plasma AVP levels were elevated despite hypoosmolality in all the 2 groups of hyponatremic, elderly patients. Plasma renin activity and plasma aldosterone concentrations were low in the patients with SIADH and central salt-wasting syndrome. Fludrocortisone acetate therapy was effective in the patients with central salt-wasting syndrome and 3 patients with SIADH whose hyponatremia remained unchanged after water restriction. Water restriction therapy normalized serum Na levels in only 3 patients with SIADH. These results indicate that AVP is involved in the mechanism for hyponatremia in the elderly patients with SIADH and central salt-wasting syndrome. Severe hyponatremia associated with SIADH and central salt-wasting syndrome responds well to mineralocorticoid therapy. Both the secretion of AVP and renal sodium handling may be involved in the mechanisms of action of the disorders. The diagnostic criteria for SIADH in the elderly patients may have to be reevaluated and should be considered to indicate fludrocortisone acetate therapy.

Abstract. We studied the changes in serum sodium (Na) and potassium (K) levels in seventeen patients in diabetic ketoacidosis and nine patients in non-ketotic hyperosmolar coma, who had marked hyperglycemia (707.4±75.6 mg/dl, mean±SEM) and dehydration. The disorder characterized two types of alteration. The one group was hyponatremia with hyperkalemia in 17 patients in diabetic ketoacidosis (132.9±2.0 and 5.7±0.2 mEq/l), and 4 patients in non-ketotic hyperosmolar coma (125.8 ±4.3 and 5.2±0.5 mEq/l). The other was hypernatremia (162.5±1.8 mEq/l) with hypokalemia (3.4± 0.2 mEq/l) in 5 patients in non-ketotic hyperosmolar coma. Intensive therapy with insulin and fluid administration improved the diabetic hyperglycemia and associated abnormalities. The vectors showing the normalization of serum Na and K levels was in quite opposite directions between the patients with hyponatremia with hyperkalemia and those with hypernatremia with hypokalemia. The amounts of loss of circulatory blood volume exceeded 20% in three groups of patients, a loss greater in the hypernatremic patients than in the hyponatremic ones. These results indicate that serious body water depletion produces hypernatremia instead of hyponatremia in patients in diabetic coma. The disorder may be caused by the altered distribution of electrolytes between the intra-and extra-cellular spaces.

The present study was undertaken to determine whether there are Ca2+ -dependent and -independent pathways of glucose-induced insulin secretion from the pancreatic beta cell line MIN6. Glucose at a concentration of 16.7 mmol/l caused marked increases in cellular free calcium ([Ca2+]i) and insulin secretion, which depended on glucose metabolism. When cells were pretreated with 20 mmol/l mannoheptulose, an inhibitor of glucokinase, the 16.7 mmol/l glucose induced a rise in [Ca2+]i and insulin secretion disappeared. Also, L-leucine and L-arginine increased [Ca2+]i and induced insulin secretion. Under Ca2+ -free conditions, insulin release was still induced, without any change in [Ca2+]i, by these three different stimulants. The cumulative values of insulin secretion were 13.7-29.3% of the control, which were significantly less than that in the presence of Ca2+. Cellular alkalinization occurred in response to all these stimulants, irrespective of the presence of Ca2+. Forskolin, a diterpene activator of adenylate cyclase, produced insulin secretion independently of [Ca2+]i, which accompanied cellular alkalinization. Also, a high glucose level increased cellular cyclic AMP (cAMP) production in the presence and absence of Ca2+, and the effect was diminished by approximately 73% in Ca2+ -free conditions. These results indicate that a high glucose level stimulates both Ca2+ -dependent and -independent insulin secretion from pancreatic beta cells. We suggest that the cAMP production and the cellular alkalinization participate in the Ca2+ -independent mechanism. Spermatogonial proliferation is under the control of FSH, whereas the survival of germ cells is dependent on Sertoli cell function. The observed rise in the number of mitotically inactive Ad-spermatogonia can be explained by a transformation of Ap-spermatogonia into resting Ad-spermatogonia.