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Biomedical subjects

H K Min

Publications and source records attributed to H K Min.

61 records · Page 4Linked to original sources
PubMed1985

The effect of glucocorticoid on 125I-insulin binding to human erythrocytes. Possible postreceptor modulation of receptor binding.

To evaluate the role of insulin receptors in the pathogenesis of insulin resistance observed in glucocorticoid excess, we measured 125I-insulin binding to circulating erythrocytes in 7 patients with Cushing's syndrome and 7 patients with adrenal insufficiency. Insulin receptor binding was higher in Cushing's syndrome and was lower in adrenal insufficiency, compared to normal subjects. Insulin binding decreased after transsphenoidal surgery in 2 patients with Cushing's syndrome. In addition, glucocorticoid treatment in 6 patients with adrenal insufficiency resulted in the increase of insulin binding. The biological significance of this phenomenon must await further investigation, but it does suggest that insulin resistance in glucocorticoid excess should be interpreted as an alteration of cellular mechanisms of insulin at a step distal to the insulin receptor. Increased insulin binding to the receptor is probably modulated by postreceptor events.

Adrenal Insufficiency↗
PubMed1984

Clonorchis sinensis: pathogenesis and clinical features of infection.

When larvae of C. sinensis reach the biliary system and mature, the flukes provoke pathological changes, both as a result of local trauma and of toxic irritation. The appearances vary with duration and severity of the infestation, but they are sufficiently distinctive and characteristic to allow a classification into four phases as follows; 1st phase, desquamation of epithelial cells, 2nd phase, hyperplasia and desquamation of epithelial cells, 3rd phase, hyperplasia and desquamation of epithelial cells, and adenomatous tissue formation, and 4th phase, marked proliferation of the periductal connective tissue with scattered abortive acini of epithelial cells and fibrosis of the wall of the bile duct. The onset of symptoms and signs is at times gradual, at times sudden. Chill and fever up to 40 degrees C occur during the acute stage, i.e. the period less than a month after parasite invasion. And a few weeks later, the chronic stage follows with the classical clinical features. In general, symptoms and signs can be classified as follows: mild, essentially symptomless, progressive, with irregular appetite, gastrointestinal disturbances, oedema, hepatomegaly, etc., and severe, with a syndrome associated with portal cirrhosis and hypertension. Pathogenic changes and complications are generally restricted to foci, but may eventually affect the whole liver. Calculi, acute suppurative cholangitis, recurrent pyogenic cholangitis, cholecystitis, hepatitis, and acute pancreatitis are important complications. Carcinoma of the liver is often found in association with clonorchiasis, too.

Clonorchiasis↗
PubMed1983

IgG heavy-chain (Gm) allotypes and HLA-antigens in insulin-dependent diabetes mellitus in Korea.

Eighty-eight patients with insulin-dependent diabetes mellitus (IDDM) and seventy-two unrelated normal controls in Korea were studied for Gm allotypes and HLA-antigens. Ten Gm phenotypes were found among the Korean population. The phenotype frequencies of Gm axg (1,2,21), Gm ag (1,21), Gm agb0b3b5st (1,21, 11,13,10,15,16) and Gm agfb0b1b3b4b5 (1,21,3,11,5,13,14,10) were higher than the other Gm allotypes, but there was no significant difference between patients and controls. HLA-BW54 was found in 15% of patients who had any of those Gm allotypes (Gm axg, Gm agb0b3b5st, Gm ab0b3b5st). However there was no significant difference in frequency as compared with controls.

Diabetes Mellitus, Type 1↗
PubMed1976

Transplacental migration of Toxocara canis larvae in experimentally infected mice.

In experimentally infected, nonpregnant mice the larvae of Toxocara canis were not found in the uterus at any time. In mice infected at 1 week, but not at 2 weeks, before gestation, larvae were found in the uterus but not in either the placenta or fetus. In mice infected during pregnancy, larvae were found in the uterus and placenta from the 9th day and in the fetus from the 11th day of pregnancy, more abundantly when infected at the middle than at the earlier stages. Examination of microsections revealed larvae in both maternal sinusoidal spaces and fetal blood vessels of the placenta; though mechanical damage to the tissues and the debris of tissues were sometimes seen, larva-associated inflammation in these tissues were not observed. The results suggest that in the pregnant mouse the migration of T. canis larvae is influenced by the developmental stages of the placenta.

Animals↗
PubMedDate not supplied

Spontaneous hypoglycemia and insulin autoantibodies in a patient with Graves' disease.

A 31-year-old woman with Graves' disease developed fasting hypoglycemia after treatment for 3 weeks with methimazole. Although the patient had not received exogenous insulin, high titers of insulin autoantibodies were found in serum and large amounts of total and free insulin (1550 and 82 microU/ml, respectively) and C-peptide reactivity (CPR, 22 ng/ml) were detected in serum. After glucose loading, blood glucose and total insulin levels increased abnormally. The immunoglobulin class of the autoantibodies was IgG and the light chains were of the kappa type. The titers of insulin autoantibodies, elevated serum total and free insulin, and CPR levels decreased gradually, but insulin autoantibodies and elevated insulin levels were still present in the serum 8 months after the episode of hypoglycemia. These findings suggest that the patient's fasting hypoglycemia was due to excess free insulin released from antibody-bound insulin, and that methimazole might play a role in the initiation of production of insulin autoantibodies.

Adult↗
PubMedDate not supplied

Glucose, insulin and C-peptide kinetics during intravenous glucose tolerance test in chronic liver disease.

To elucidate the mechanism of glucose intolerance in chronic liver disease (CLD), the kinetics of plasma glucose, insulin and C-peptide were studied after intravenous glucose loading in patients with CLD. Fasting plasma insulin levels were higher in patients with CLD than in normal subjects. This hyperinsulinemia was attributed primarily to an increased pancreatic secretion of insulin. Patients with CLD were divided into two groups, one with normal fasting plasma glucose (FBS less than 100 mg/dl (Group I) and the other with higher FBS (Group II). In Group I, the glucose disappearance rate was normal and a brisk acute insulin response (AIR) to glucose was noted. The glucose disappearance rate in Group II was lower than that in normal subjects, and AIR to glucose was blunted. It is suggested that normal glucose tolerance in Group I patients could be interpreted as a state of compensation by hypersecretion of insulin. On the other hand, the glucose intolerance in Group II patients could be due to inadequate insulin secretion to overcome insulin resistance of CLD.

Adult↗