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OBJECTIVE--To clarify mortality and morbidity of intensively managed elderly diabetic individuals and to explore factors predicting mortality and diabetes-related end points. RESEARCH DESIGN AND METHODS--A total of 390 elderly (≥65 [...]

Nutrient augmentation of [Ca.sup.2+]-triggered insulin release occurs in an ATP-sensitive [K.sup.+] ([K.sub.ATP]) channel-independent manner. Here, using rat islets, we explored the possibility of the [K.sub.ATP] channel-independent nutrient triggering of insulin [...]

We describe 4 patients with Graves disease who had abnormal increases of serum creatine kinase (CK) concentrations during treatment with antithyroid medications. Three of the patients experienced myalgia and muscle cramps. All of the patients manifested an increase in serum CK levels 1 to 3 months after the administration of antithyroid drugs. Thyrotropin concentrations and cardiac systolic time indexes during the elevation of serum CK concentrations were not consistent with hypothyroidism. The mechanisms are not obvious, but it is likely that the rapid decrease of thyroid hormones in tissues may temporarily cause hypothyroid states, resulting in alterations in CK concentrations. It is suggested that hasty correction of thyrotoxicosis should be avoided in susceptible patients, unless the thyrotoxic conditions are critical.

PURPOSE: The purpose of this study was to elucidate the mechanism of regulation of serum thyroglobulin concentration in patients with Graves' disease and to establish the clinical usefulness of this measurement. PATIENTS AND METHODS: Serum thyroglobulin concentration was analyzed in relation to serum thyrotropin receptor antibody (TRab) titer and thyrotropin concentration in 166 patients with Graves' disease without thyroglobulin antibody. RESULTS: A total of 113 patients were treated and had been kept euthyroid for at least 10 months with methimazole and underwent a triiodothyronine (T[.sub.3]) suppression test. At the time of the T[.sub.3] suppression test, the serum thyroglobulin concentration ng/mL) was 33 [+ or -] 31 in 80 of them with T[.sub.3]-suppressible (radioiodine uptake less than 12%) thyroids, negative TRab titers (less than 15% displacement), and normal serum thyrotropin concentrations (0.1 to 3.0 mU/L). Patients with T[.sub.3]-nonsuppressible thyroids were divided into three subgroups according to serum TRab titers and thyrotropin concentrations: those with a negative TRab titer and a normal serum thyrotropin concentration (n = 9), those with a positive TPab titer and a normal thyrotropin concentration (n = 18), and those with a positive TRab titer and undetectable thyrotropin (n = 6). Serum thyroglobulin concentrations (ng/mL) were 116 [+ or -] 40 in the first group, 249 [+ or -] 194 in the second group, and 399 [+ or -] 205 in the third group. In the other 39 methimazole-treated patients, 72 determinations of serum thyroglobulin concentration were performed either before or during treatment without the T[.sub.3] suppression test, and it correlated well with the TRab titer but not with the serum thyrotropin concentration. In 14 patients who became hypothyroid due to excess methimazole, the serum thyroglobulin concentration increased concurrently with elevation of the serum thyrotropin concentration and normalized during thyroxine supplementation. In treated patients with T[.sub.3]-suppressible thyroids, the serum thyroglobulin concentration was similar among those with positive (n = 54) and negative (n = 26) microsomal antibody, indicating that the presence of Hashimoto's thyroiditis does not profoundly affect the serum thyroglobulin level. Among 80 patients with T[.sub.3]-suppressible thyroids who were followed without methimazole for a mean period of 31.1 months, eight (10%) experienced a clinically overt recurrence of hyperthyroidism. Serum thyroglobulin concentration and TRab titer %) in these eight patients were 188.1 [+ or -] 101.7 and 27.8 [+ or -] 12.6, respectively. Thyroglobulin and TRab did not increase in the patients who remained euthyroid (n = 71) or who experienced subclinical recurrence (n = 1). CONCLUSIONS: Abnormal thyroid stimulator(s) and thyrotropin synergistically (if both are present in the serum) or independently (if either one is present) stimulate thyroglobulin secretion in patients with Graves' disease. Therefore, serum thyroglobulin concentration can be a useful means of assessing the degree of thyroidal stimulation and, if serum thyrotropin is normal or suppressed, correlates well with thyroidal stimulation even in patients with a negative TRab titer., Graves' disease is characterized by an enlarged thyroid gland and abnormal protrusion of the eyeballs. The regulation of blood levels of thyroglobulin, an iodine-containing protein released by the thyroid gland, was assessed in patients with Graves' disease. Thyroglobulin levels were assessed in relation to levels of the pituitary hormone thyrotropin, which stimulates the thyroid gland, and the presence of antibodies, or immune proteins, that specifically bind to receptors for thyrotropin (TRab). One hundred and thirteen patients were treated with the antithyroid drug methimazole and their thyroid activities were maintained at normal levels for at least 10 months. Blood levels of thyroglobulin averaged 116 nanograms per milliliter (ng/mL) in nine patients with normal thyrotropin levels and no TRab, 249 ng/mL in 18 patients with TRab but normal thyrotropin levels, and 399 ng/mL in six patients with TRab and undetectable thyrotropin levels. In another 39 patients treated with methimazole, thyroglobulin levels were correlated with the levels of TRab but not thyrotropin. Among 14 patients with hypothyroidism or low thyroid activity due to excessive treatment with methimazole, thyroglobulin levels increased with rising thyrotropin levels, but became normal with supplements of the thyroid hormone thyroxine. Among eight patients with recurrent hyperthyroidism or increased activity of the thyroid gland, thyroglobulin measured 188 ng/mL and TRab at almost 28 percent. Patients with normal thyroid activity or mild recurrence of hyperthyroidism maintained low levels of thyroglobulin and TRab. These findings suggest that thyrotropin and abnormal factors that stimulate the thyroid gland control the release of thyroglobulin in patients with Graves' disease. Measurement of thyroglobulin levels provides a means of assessing the activity of the thyroid gland. (Consumer Summary produced by Reliance Medical Information, Inc.)

In 1995, we reported islet cell antibody (ICA)-negative ketoacidosis (DKA)-onset diabetes with subsequent non-insulin dependency (1), which may be classified as non-autoimmune type 1 diabetes (type 1, idiopathic), or acute-onset [...]

Grb2-associated adaptor protein-1 (Gab1) is a member of the family of IRS-1-like multisubstrate docking proteins. Gab1 is tyrosine phosphorylated in response to insulin stimulation, and associates with phosphatidylinositol 3-kinase and [...]

It is well known that insulin not only regulates glucose transport and metabolism in target tissues such as the muscle but also induces cell proliferation in many cell types. Insulin [...]

Nutrients stimulate insulin release from pancreatic [Beta]-cell both through the ATP-sensitive [K.sup.+] channel-independent and -dependent mechanisms, which are most likely interrelated. Although little is known of the molecular basis of [...]

Glucose stimulation of insulin release is not solely mediated by elevation of [[[Ca.sup.2+]].sub.i] as such glucose potently augments insulin release even under [Ca.sup.2+]-free conditions. In view of this newer finding, [...]

Early intervention of diabetes is recommended for achievement of improved prognosis. However, clinical evidence supporting it is totally lacking. To evaluate the value of early intervention in type 2 diabetes, [...]

A Study in Rat Pancreatic Islets Nutrients such as glucose stimulate insulin release from pancreatic [Beta]-cells through both ATP-sensitive [K.sup.+] channel-independent and -dependent mechanisms, which are most likely interrelated. Although [...]

Free Fatty Acids Mimic ATP-Sensitive [K.sup.+] Channel-Independent Insulinotropic Action of Glucose Glucose augments [Ca.sup.2+]-stimulated insulin release from the pancreatic Β-cell in an ATP-sensitive [K.sup.+] channel ([K.sub.ATP] channel)-independent manner. In studying [...]

Regarding the mechanism of diabetic vascular complications, hyperglycemia itself is undoubtedly a major risk factor. In addition, the role of hyperinsulinemia for development of coronary atherosclerosis and peripheral vascular disease [...]

Cyclic AMP potentiates glucose-stimulated insulin release by actions predominantly at a site, or sites, distal to the elevation of the cytosolic free [Ca.sup.2+] concentration ([[Ca.sup.2+].sub.i]). Glucose also acts at a [...]

Insulin release by freshly isolated single rat pancreatic islets was systematically analyzed for the first time. The islets showed a concentration-dependent, not all or none, response to the stair-case glucose [...]

It is well established that impaired glucose tolerance (IGT) is a risk for developing diabetes, so that the important purpose of performing a screening of glycemia in general population is [...]

Treatment of the human hepatoma (HepG2) cells with high glucose (33 mM) caused phosphorylation of serine residue of insulin receptor substrate1 (IRS-1). At the same time, the high, glucose treatment [...]

We have encountered 9 patients (6 men and 3 women, aged 16 to 36 yrs) with acute onset diabetic ketosis or ketoacidosis without precipitating illness, in whom ICA and/or [Alpha]GAD [...]

Recently, hypoadiponectinemia was found to be associated with coronary artery disease in humans (1). Conversely, hyperadiponetinemia caused by a transgenic overexpression of the adiponectin gene prevented atherosclerosis in the mouse [...]