Biomedical subjects

L T Ho

Publications and source records attributed to L T Ho.

At least 127 records · Page 7Linked to original sources

PubMed1990

Insulin insensitivity in offspring of parents with type 2 diabetes mellitus.

Measurements were made of the plasma glucose and insulin responses to a 75 g oral glucose challenge in 50 Chinese born in Taiwan, divided into two groups on the basis of family history of Type 2 diabetes. Twenty-five individuals (age 29 +/- 5 (+/- SD) years) had 2 parents with normal oral glucose tolerance, whereas at least 1 parent had Type 2 diabetes in the other 25 subjects (age 30 +/- 6 years). In addition, in vivo insulin action was estimated by determining the steady-state plasma glucose concentration during a 3-h continuous infusion of glucose, insulin, and somatostatin. Steady-state plasma glucose concentration was used as a measure of insulin-induced glucose disposal. The 50 subjects were non-obese, and of comparable gender distribution and body mass index. Plasma glucose and insulin concentrations in response to oral glucose were similar in the two groups. However, the steady-state plasma glucose concentration was significantly (p less than 0.01) higher in offspring with a family history of Type 2 diabetes when compared by two-way analysis of variance (mean +/- SE was 5.87 +/- 0.27 vs 5.12 +/- 0.32 mmol l-1). This difference was found despite a significantly (p less than 0.01) higher steady-state plasma insulin concentration during the infusion studies (0.705 +/- 0.027 vs 0.643 +/- 0.025 nmol l-1) in offspring of people with diabetes. The results support the view that resistance to insulin-stimulated glucose uptake is present in offspring of diabetic parents.

Adult↗

PubMed1990

Changes of insulin receptor in aortic endothelial cells from diabetic rats.

Endothelial cells are likely to play an important role in the development of diabetic vascular diseases since they are exposed directly to the abnormal circulating metabolites of diabetes and may be easily damaged early in the natural course of vascular complications. Recently, we have demonstrated a decrease of insulin binding and autophosphorylation of the insulin receptor in cultured capillary endothelial cells of diabetic rats. In this study, similar defects in insulin receptor of aortic endothelial cells cultured from diabetic BB rats were found. The specific insulin binding was 45% lower in cells from diabetic than from non-diabetic rats (3.9 +/- 1.3 vs 7.3 +/- 1.2% per mg protein, p less than 0.05), which was due to a decrease of cell surface binding sites. In contrast to the decrease in insulin binding, insulin-like growth factor-I binding was higher in cells of diabetic than control rats (20.6 +/- 5.6 vs 13.7 +/- 4.6% per mg protein). The decrease in insulin binding could not be induced by the two-week treatment of endothelial cells from non-diabetic rats with medium containing high concentration of glucose (400 mg/dl). Insulin-induced tyrosine kinase activity of partially purified insulin receptor measured using poly-glutyr as substrate was also lower in cells from diabetic rats (normal:1.4 +/- 0.6-fold; diabetic 0.5 +/- 0.3-fold above baseline; (p less than 0.05). These data suggest that the diabetic milieu in vivo can induce persistent defects in insulin receptor of aortic endothelial cells. Further studies are warranted to understand the potential pathophysiological role of these defects.

Animals↗

PubMed1990

Fanconi syndrome: report of a case.

A 59-year-old female patient was admitted because of muscle weakness in all four limbs for a period of 5 days. She had been found to have Graves' disease 4 years ago previous to this, and had received a subtotal thyroidectomy 1 year later. Hypothyroidism supervened and she had been receiving levothyroxine replacement in recent years. She also had non-insulin-dependent diabetes, which was controlled with diet only. During the 5 days prior to admission, she developed muscle weakness which finally worsened to complete paralysis of all four limbs. Physical examination showed tenderness and weakness of the extremity muscles. Abnormal laboratory data included serum K, 1.6 mEq/L; P, 1.2 mg/dl; uric acid, 1.6 mg/dl; fasting glucose, 267 mg/dl; T3, 36.65 ng/dl; T4, 4.0 micrograms/dl; TSH, 5.35 mu u/ml; free T4, 0.57 ng/dl; and metabolic acidosis with pH, 7.298; PCO2, 27.0 mmHg; and HCO3, 12.8 mEq/L. An EKG showed a prominent U wave, and urinalysis revealed renal glucosuria and massive aminoaciduria. An oral sodium bicarbonate loading test showed an increasing loss of bicarbonate through the urine, while the plasma bicarbonate level was elevated. Clinical manifestations improved after the administration of sodium bicarbonate, potassium chloride and neutral phosphate.

Autoimmune Diseases↗

PubMed1990

Intractable diabetic ketoacidosis due to insulin antibody--response to steroid therapy.

To examine the effect of steroid therapy on insulin antibody titer in insulin-dependent diabetes mellitus, we studied a 58 year-old gentleman with recurrent diabetic ketoacidosis. No any overt precipitating factors could be accounted for, except limited pancreatic beta cell reserve and high titers of anti insulin antibodies. Despite the persistence of high titers of plasma antiinsulin antibodies, the clinical manifestations of diabetic ketoacidosis improved greatly by the administration of steroid. Nevertheless, the patient still showed the great excursion of plasma glucose concentration.

Diabetes Mellitus, Type 1↗

PubMed1990

Thyrotropin-and prolactin--secreting pituitary tumor dissociated hormonal response to bromocriptine.

A 41-year-old male with recurrent hyperthyroidism resulting from pituitary tumor was studied. Because of recurrent hyperthyroidism, he had been treated with propylthiouracil for four years and had been operated. At the time of high serum thyroid hormone (T4: 20 micrograms/dl; T3:502 ng/dl), there was also elevated basal serum TSH level (55 microU/ml) which could not be suppressed by exogenous thyroid hormone administration. In addition, the serum TSH showed blunt response to intravenous TRH infusion. An elevated serum prolactin level was also observed (111 ng/ml). After bromocriptine administration (2.5 mg daily), the suppressibility of serum TSH level was found better than that of prolactin level. The existence of a TSH- and PRL-secreting pituitary tumor in this patient exhibited a dissociated hormonal response to low doses of dopaminergic agents.

Adult↗

PubMed1990

An in vitro approach to the kinetics of insulin antibodies in diabetic patients.

The purpose of this study is to evaluate the binding behavior of plasma insulin antibodies (Iab) in diabetic patients, by the following parameters: Incubation time, temperature, buffer pH, and Iab titer. We investigated the plasma insulin binding patterns of 12 insulin-treated diabetic patients, and they were separated as higher titer group (Iab = 51.9 +/- 7.28, n = 6) and lower titer group (Iab = 14.88 +/- 4.75, n = 6). The procedure was: (1) plasma samples were deinsulinized by 0.12N HCL, dextran coated charcoal suspension and 0.12N NaOH. (2) I-125 monoiodoinsulin was used to prevent artifacts resulting from variability in ligand binding due to excessive iodination, (3) separation of free and bound insulin was accomplished by rapid precipitation of hormone-antibody complex with polyethylene glycol, and (4) decanting the supernatants and counting the pellets in the automatic gamma counter. The data were obtained as the condition of incubation time, temperature, buffer pH, and Iab titer. The results obtained by the Scatchard analysis indicated that high temperature (39 degrees C vs 37 degrees C) in vitro would increase the free insulin levels and decrease the low affinity binding capacity (Q2-Q1) of Iab in patients with high titer of Iab (greater than 40%), whereas this phenomenon is not observed in patients with low affinity binding sites of Iab in patients with low titers of insulin antibodies (less than 20%).

Antigen-Antibody Reactions↗

PubMed1990

Comparison of insulin secretion and insulin sensitivity between normal and impaired glucose tolerance subjects with normal fasting plasma glucose.

To examine glucose-stimulated insulin secretion and insulin sensitivity in the normal subjects and patients with impaired glucose tolerance, we performed the oral glucose tolerance test (OGTT) and modified insulin suppression test in 34 non-obese subjects. The plasma glucose and insulin concentrations were measured during fasting and every 30 min up to 120 min following 75 g of oral glucose loading. Ten subjects were classified as impaired glucose tolerance (IGT), and 24 subjects were as having normal glucose tolerance. In addition, the insulin-stimulated glucose uptake was estimated in all subjects by measuring the final 30 min steady-state plasma glucose (SSPG) of a continuous infusion of somatostatin, insulin and glucose for 4 hours (modified insulin suppression test). The mean plasma glucose concentrations of fasting and 60, 90, 120 min during OGTT study were significantly higher in the IGT subjects than in the normals. In addition, the mean incremental glucose areas under the curve during OGTT study were also greater in the IGT subjects than in the normals. The mean serum insulin concentrations were significantly higher at 90 and 120 minutes in the IGT patients than in the normals. During the modified insulin suppression test, the mean SSPG concentrations were significantly higher in the IGT patients than in the normals under the similar steady-state plasma insulin in both groups. There was a good correlation between the incremental insulin areas under the curve (OGTT) and the SSPG in the normal subjects (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

The action of gliclazide on insulin secretion and insulin sensitivity in non-obese non-insulin dependent diabetic patients.

We evaluated the effects of gliclazide on the secretion and action of insulin in 18 non-obese (BMI 24.09 +/- 0.47 Kg/m2, range 20.89-27.52 Kg/m2) non-insulin dependent diabetic patients (mean age 56.9 +/- 1.8 years, range 39-67 years) by the oral glucose tolerance test (OGTT) and insulin suppression test (IST). Most of them were diagnosed recently and thus untreated previously. All subjects were treated with gliclazide or placebo for 3 months in a double blind cross-over design. After gliclazide therapy, fasting and 2 hour post-OGTT plasma glucose significantly decreased (136 vs. 185 mg/dl, P less than 0.005 291 vs. 358 mg/dl, P less than 0.005), 2 hours post-OGTT plasma insulin was significantly increased (79 vs. 59 uU/ml, P less than 0.05) while fasting plasma insulin remained unchanged (21 vs. 19 uU/ml, P greater than 0.1). HbAlc decreased significantly with gliclazide therapy (6.6 vs. 7.6%, P less than 0.005). In addition, oral glucose tolerance, as measured by the mean incremental areas under the plasma glucose curve, were improved significantly (1430.6 +/- 682.4 vs. 16192.5 +/- 608.5 mg.min/dl, P less than 0.005). The mean incremental areas under the plasma insulin curve during OGTT also increased (4482.0 +/- 637.1 vs. 3167.5 +/- 511.9 uU.min/ml, P less than 0.05) after gliclazide therapy. Mean steady state plasma glucose levels (SSPG) showed no remarkable difference during drug and placebo administration (188 vs. 190 mg/dl). Throughout the trial there was no significant change of body weight, nor any side effect as judged from blood counts, urinalysis, and the results of SMA-23 and EKG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Coexisting hyperthyroidism and hyperparathyroidism: two cases report.

To examine the biochemical changes in coexisting hyperthyroidism and hyperparathyroidism, we have studied two female cases in our medical center. Both patients received biochemistry study, thyroid function test, thyroid autoantibody determination, parathyroid function tests and thyroid scan. They all had increased thyroid function. The concentration of parathyroid hormone was found to elevate in both cases. After thyroid function turned normal, hypercalcemia was still present. Both patients underwent neck operation. Parathyroid adenoma was found in both cases. The pictures of thyroid pathology showed diffuse hyperplasia in one case and lymphocytic thyroiditis in the other case.

Adenoma↗

PubMed1990

Severe rhabdomyolysis induced acute renal failure, caused by diabetic ketoacidosis.

A 23 year-old obese Chinese gentleman was admitted to our hospital with the main problem of conscious disturbance for one day. The physical examination and laboratory data confirmed that this is a case of diabetic ketoacidosis complicated with rhabdomyolysis resulting in acute renal failure three days after admission, and regained his renal function after intensive hemodialysis and other conservative treatment.

Acute Kidney Injury↗

PubMed1990

Insulin secretion and sensitivity in acromegaly.

To examine the effect of excess growth hormones on carbohydrate metabolism, we studied glucose-stimulated insulin secretion and glucose utilization in 6 patients with acromegaly and 6 age-, sex- and weight-matched normal subjects. The levels of plasma glucose and serum insulin were determined during fasting and every 30 min up to 180 min after 75 g of oral glucose loading. In addition, plasma glucose, serum insulin and serum C-peptide were measured during euglycemic glucose clamp with insulin infusion of 40 mU/m2,min-1. The acromegalic patients had significantly higher mean levels of fasting plasma glucose (p less than 0.05) and insulin (p less than 0.01). After glucose loading for 3 h, the acromegalic patients also had a higher incremental area under the curve of plasma glucose (p less than 0.05) and serum insulin (p less than 0.05). However, no significant difference in the fasting molar ratio of C-peptide/IRI was noted between these two groups. During euglycemic clamp studies, the steady-state serum insulin levels were identical between the two groups. The glucose disposal rate was lower in acromegalics than in normal subjects (p less than 0.01). The results demonstrated that glucose intolerance, hyperinsulinemia and insulin resistance are present in acromegalic patients.

Acromegaly↗

PubMed1989

Hyperparathyroidism presenting as a large bone tumour. A case report.

A 59-year-old man, who presented to hospital with a large expansile bone tumour over the left elbow and a mass in the right side of the neck, was eventually found to have parathyroid adenoma manifesting clinically as severe hypercalcaemia. Histological examination of a section of the neck mass showed parathyroid adenoma and the bone biopsy specimen revealed a 'brown tumour', consistent with hyperparathyroid bone disease.

Adenoma↗

PubMed1989

The hypothalamic somatostatinergic pathways mediate feeding behavior in the rat.

The level of somatostatin in the hypothalamus was higher in satiated rats than in hungry rats. Elevating hypothalamic somatostatin levels by administering somatostatin into the hypothalamus produced a decrease in food intake, whereas lowering hypothalamic somatostatin levels by administering cysteamine into the peritoneal cavity produced an increase in food intake in rats.

Animals↗

PubMed1989

Insulin induces activation of kinase FA in membranes and thereby promotes activation of ATP.Mg-dependent phosphatase in adipocytes.

Exposure of rat adipocytes to physiological concentrations of insulin resulted in a time- and concentration-dependent activation-translocation of kinase FA (an activating factor of ATP.Mg-dependent protein phosphatase) in plasma membranes and the subsequent activation of ATP.Mg-dependent protein phosphatase in the cytosol. The insulin-induced activation of membrane-associated kinase FA and cytosolic ATP.Mg-dependent protein phosphatase occurred very rapidly, reaching the maximal activity levels within 3 min. Moreover, the insulin effect is transient; the insulin-stimulated FA activity in membranes and ATP.Mg-dependent phosphatase activity in the cytosol returned to control levels within 30 min. It is concluded that insulin may induce the activation of kinase FA in membranes and thereby promotes the activation of ATP.Mg-dependent multifunctional protein phosphatase in the cytosol of rat adipocytes in order to mediate some of its intracellular effects through the dephosphorylation reactions. The release of factor FA from plasma membranes may represent one of the transmembrane signalling mechanisms for insulin actions.

Adenosine Triphosphate↗

PubMed1989

Hypothalamic somatostatin may mediate endotoxin-induced fever in the rat.

(1) The changes in rectal temperature produced by an injection of a bacterial endotoxin piromen (10-40 ng in 1.0 microliter) on somatostatin-14 (SS-14; 0.1-0.3 microgram in 1.0 microliter) into the preoptic anterior hypothalamic area were assessed and compared in control rats, in rats with hypothalamic SS depletion, and in rats with hypothalamic SS receptor blockade. (2) Intrahypothalamic injection of either piromen or SS-14 produced a dose-related rise in rectal temperature in intact, control rats. The fever induced by intrahypothalamic injection of piromen or SS-14, as well as that induced by intraperitoneal injection of piromen, was antagonized by pretreatment of the hypothalamus with a SS-14 receptor antagonist (0.1 ng in 1.0 microliter) in rats. (3) On the other hand, intraperitoneal administration of cysteamine (30-100 mg/kg), in addition to producing a dose-related fall in rectal temperature, also caused a dose-related fall in hypothalamic SS-levels in rats. Furthermore, the fever induced by intrahypothalamic injection of piromen, but not SS-14, was antagonized by depletion of hypothalamic SS levels with an intraperitoneal dose of cysteamine (30 mg/kg). (4) The results indicate that a somatostatinergic pathway in the hypothalamus may mediate endotoxin-induced fever in the rat.

Animals↗

PubMed1989

Somatostatin: a hypothalamic transmitter for thermoregulation in rats.

The changes in both the thermoregulatory responses and brain somatostatin (SS) levels produced by ambient temperature (Ta) changes were assessed in rats after they had been equilibrated to each of the Ta for a period of about 90 min. Cold exposure, in addition to elevating hypothalamic SS-levels, led to increased metabolism and cutaneous vasoconstriction at Ta = 8 degrees C. In contrast, heat exposure, in addition to lowering hypothalamic SS-levels, resulted in decreased metabolism and cutaneous vasodilation at Ta = 30 degrees C. Rats were chronically implanted with a hypothalamic cannula to allow intrahypothalamic injection of SS on the conscious rats. Direct administration of SS (0.1-0.3 micrograms) into the preoptic anterior hypothalamic area caused a dose-related rise in colon temperature at three Ta tested. The SS-induced hyperthermia was produced by increased metabolism at Ta = 8 degrees C, whereas at Ta = 30 degrees C, it was caused by cutaneous vasoconstriction. At Ta = 22 degrees C, the hyperthermia was caused by increased metabolism and cutaneous vasoconstriction. Systemic administration of cysteamine, in addition to lowering hypothalamic SS-levels, produced a dose-related fall in colon temperature at Ta of 8 degrees C and 22 degrees C. The hypothermia induced by cysteamine was produced by decreased metabolism at Ta = 8 degrees C, whereas at Ta = 22 degrees C, it was caused by both decreased metabolism and cutaneous vasodilation. The data indicate that the hypothalamic SS-levels mediate normal body temperature responses in rats.

Animals↗

PubMed1989

Insulin secretion and sensitivity in hyperthyroidism.

To examine the effect of hyperthyroidism on carbohydrate metabolism, we studied glucose-stimulated insulin secretion and glucose utilization in 8 subjects with Graves' disease before and after treatment for hyperthyroidism and 8 age-, sex- and weight-matched normal subjects. Subjects with Graves' disease had significant elevated serum levels of thyroxine (24.81 +/- 2.44 micrograms/dl, mean +/- SEM) and triiodothyronine (459 +/- 5.5 ng/dl, mean +/- SEM). Simultaneous measurement of plasma glucose, serum insulin and C-peptide levels during fasting and every 30 minutes up to 180 minutes after 75 g oral glucose loading was determined. In addition, plasma glucose, serum insulin and serum C-peptide were measured during euglycemic glucose clamp with insulin infusion of 40 mU/m2 min-1. Mean fasting plasma glucose (P less than 0.05, serum insulin (P less than 0.005) and serum C-peptide (P less than 0.005) levels were significantly higher in the hyperthyroid patients. After glucose loading, the plasma glucose (P less than 0.05), serum insulin (P less than 0.05) and C-peptide (P less than 0.05) responses were significantly higher in hyperthyroid patients at all times up to 180 minutes. During euglycemic clamp studies, the steady-state serum insulin levels were identical in the two groups. The glucose disposal rate was lower in hyperthyroid patients before treatment (P less than 0.01) than in normal subjects. After thyroid function had been normalized for 2 to 4 weeks, the glucose disposal rate increased significantly (P less than 0.05), but was still significantly lower than those of normal subjects (P less than 0.05). Our data show that patients with Graves' hyperthyroidism manifest glucose intolerance, hyperinsulinemia and insulin resistance.

Administration, Oral↗

PubMed1989

Effect of habitual physical activity on age-related glucose intolerance.

Plasma glucose and insulin responses to a standard oral glucose challenge and a mixed meal were determined for two groups of male volunteers (office workers and laborers) and a group of female housewives or office workers. Although glucose tolerance declined with age to a certain degree in all three groups, the age-related change varied as a function of both level of habitual physical activity and gender. Specifically, the decline in glucose tolerance was greatest in the male office workers and least in the females. The plasma insulin responses did not increase with age in any of the groups. These results suggest that glucose tolerance decreases with age because there is a decline in insulin action, which is not compensated for by an increase in insulin secretion. Insulin sensitivity appears to be enhanced in females as compared with males. Sensitivity is also enhanced in males habitually engaged in physical labor; thereby accounting for the age-related decline being greatest in the male office workers. Finally, the results showed that although the loss of glucose tolerance with age varied from group to group, the quantitative nature of the change was modest in all three groups. These data further emphasize that very little change in glucose tolerance is associated with aging in generally healthy, nonobese individuals.

Adult↗