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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uncontrollable change of diabetes mellitus (DM) has occurred in one of our patients who had received hepatic arterial embolization (HAE) for hepatocellular carcinoma (HCC). This prompted us to examine the influence of HAE to the diabetic patients with HCC. Thirty-four patients accompanying DM who had received HAE were examined fasted blood glucose (FBG) and the liver function before and after the procedure. HAE was performed using Gelatin Sponge and Lipiodol containing anticancer agents, either alone or combined. Of 34 patients 6 showed increase of FBG level of more than two times after HAE. The FBG level had a tendency to elevate as the grade of DM advanced. The tendency was also recognized on pre-HAE oral glucose tolerance test. However, FBG elevation had no relation to the changes of liver function (GPT, Choline Esterase), the difference of embolic materials and pre-HAE status of DM control. From the results, one must be aware that HAE or Lipiodol infusion to diabetic patients with HCC sometimes may cause uncontrollable change of DM, especially in case of advanced DM patients. Consequently, careful follow-up of HCC as DM is advisable for improvement of the patients' prognosis.
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PMID:[Influence of hepatic arterial embolization on diabetic patients with hepatocellular carcinoma]. 255 88

At least two genetically distinct glucose transporters (GTs) coexist in adipose cells, one cloned from human hepatoma cells and rat brain (HepG2/brain) and another from rat skeletal muscle, heart, and adipose cells (adipose cell/muscle). Here we demonstrate differential regulation of these two GTs in adipose cells of diabetic and insulin-treated diabetic rats and compare changes in the expression of each GT with marked alterations in insulin-stimulated glucose transport activity. Adipose cell/muscle GTs detected by immunoblotting with the monoclonal antiserum 1F8 (James, D. E., R. Brown, J. Navarro, and P. F. Pilch. 1988. Nature (Lond.). 333:183-185), which reacts with the protein product of the newly cloned adipose cell/muscle GT cDNA, decrease 87% with diabetes and increase to 8.5-fold diabetic levels with insulin treatment. These changes concur qualitatively with previous detection of GTs by cytochalasin B binding and with insulin-stimulated 3-O-methylglucose transport. Northern blotting reveals that the adipose/muscle GT mRNA decreases 50% with diabetes and increases to 6.8-fold control (13-fold diabetic) levels with insulin treatment. In contrast, GTs detected with antisera to the carboxyl terminus of the HepG2 GT or to the human erythrocyte GT show no significant change with diabetes or insulin treatment. The HepG2/brain GT mRNA is unchanged with diabetes and increases threefold with insulin treatment. These results suggest that (a) altered expression of the adipose cell/muscle GT forms the molecular basis for the dysregulated glucose transport response to insulin characteristic of diabetes, (b) the expression of two types of GTs in rat adipose cells is regulated independently, and (c) alterations in mRNA levels are only part of the mechanism for in vivo regulation of the expression of either GT species.
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PMID:Differential regulation of two glucose transporters in adipose cells from diabetic and insulin-treated diabetic rats. 266 32

Clinical and pathological analysis of 66 cases of fibromatoses are presented. The age range in our series was 1 to 72 years. Superficial fibromatoses occurred predominantly in older patients with a peak incidence in the fifties while deep fibromatoses occurred predominantly in younger patients with a peak incidence in the twenties. Male to female ratio was 1.4 to 1. The abdominal fibromatosis occurred in female while our palmar fibromatosis occurred in male. There were 17 cases (26%) of multiple fibromatoses which occurred most frequently on both palms and had a tendency to symmetric distribution. The latent period between the two fibromatoses in a patient ranged from 1 year to 36 years. Clinical presentations included a palpable nodule or mass; flexure contracture of finger; penile hypertrophy, contracture, or discomfort on erection; and soreness, tenderness, or paresthesia over the tumor. Hydronephrosis may be complicated by intraabdominal fibromatosis. Size of the tumors ranged from 0.5 cm. To 30.0 cm. Three cases were associated with diabetes mellitus, 2 with alcoholics, 1 with liver cirrhosis, 2 with pulmonary tuberculosis, and 3 with hepatocellular carcinoma, cholangiocarcinoma, and mammary papillary carcinoma, respectively. Nine cases (14%) were associated with variable types of trauma, including being hurt by a stick, intramuscular injection in the gluteal region, tying penile shaft with a plastic band, breast massage and hot applying, and operation on abdomen. The superficial fibromatoses seldom recurred after excisional biopsy or fasciectomy while the deep fibromatoses often recurred. The recurrent rate of the deep fibromatoses was 21%. Malignant transformation or spontaneous regression was not found.
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PMID:[The fibromatoses. A clinicopathological study of 66 cases]. 281 66

In view of the increasing incidence of primary hepatocellular carcinoma in western Europe and concern that this may in part be related to long-term use of drugs which cause hepatic microsomal enzyme induction, we undertook a comparison of long-term drug use in 105 patients with hepatocellular carcinoma and equal numbers of age and sex-matched patients with colorectal tumours and with fractures of femur. We found no patients with hepatocellular carcinoma who were long-term anticonvulsant users and only one who used oral contraceptives. However, we observed a four-fold excess of diabetic patients among the group with hepatocellular carcinoma. This association did not appear to be due to pre-existing haemochromatosis, alcoholic cirrhosis or viral hepatitis. The association was strongest in patients receiving drug treatment for diabetes, but the data, although suggestive, were insufficient to determine whether any specific anti-diabetic agent could be responsible. Further studies are required to elucidate the nature of this unexpected association. An association of this magnitude with diabetes mellitus could account at least in part for the increasing incidence of hepatocellular carcinoma in western Europe.
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PMID:Diabetes mellitus and primary hepatocellular carcinoma. 281 32

A study of insulin-receptor internalization and recycling was undertaken in primary cultures of rat hepatocytes and a human hepatoma cell line (HepG2). Receptors were quantitated by measuring 125I-insulin binding to partially purified soluble receptor preparations from untreated cells (total receptors) and trypsinized cells (intracellular receptors). In resting HepG2 cells, exposure to insulin results in internalization of insulin receptors, the rate and extent of which is dependent on the insulin concentration. However, receptors do not accumulate inside the cell in proportion to the higher rates of internalization at high concentrations of insulin. This lack of accumulation is explained by much higher recycling rates after exposure to high concentrations of insulin. Similar results were noted for primary cultures of rat hepatocytes. These results imply qualitatively different fates for receptors internalized after exposure to different concentrations of insulin. To further investigate the possibility of different pathways for insulin-receptor internalization and processing, cells in low (1 ng/ml) or high (100 ng/ml) concentrations of insulin were exposed to drugs or treatments known to affect receptor metabolism. Hypotonic shock and hypokalemia, which arrest coated-pit formation, blocked internalization of insulin and insulin receptors at low concentrations of insulin but allowed internalization in response to high concentrations of insulin. The lysosomotropic drugs monensin and chloroquine caused intracellular accumulation of insulin and its receptors internalized at low concentrations of insulin but had a relatively smaller effect on receptors internalized at high concentrations of insulin. All internalization is blocked by 2,4-dinitrophenol. We conclude that high doses of insulin lead to insulin-receptor internalization and recycling through a pathway that is functionally distinct from the pathway taken by receptors internalized by low (physiologic) concentrations of insulin. The pharmacologic experiments raise the possibility that the high-dose pathway, unlike the low-dose pathway, may proceed independently of coated pits and endosomal acidification.
Diabetes 1988 Jun
PMID:Evidence for two independent pathways of insulin-receptor internalization in hepatocytes and hepatoma cells. 283 54

A case-control study was carried out to explore possible risk factors of primary hepatocellular carcinoma (PHC) in Taiwan. One hundred thirty-one PHC patients and 207 hospital control patients were interviewed and blood samples were collected for blood type and hepatitis B virus (HBV) infection marker tests. Eighty-three percent of the PHC patients were found to be hepatitis B surface antigen (HBsAg) positive as compared with 21.0% of the control patients with an odds ratio (OR) of 21.5. Hepatitis B e antigen (HBeAg) positive status increased the risk of PHC. No significant association was observed between erythrocyte genetic markers and PHC, except c of the Rh system, which was significantly lower in the PHC cases. As compared with the control patients, the PHC patients had a higher proportion with a history of liver diseases and more siblings affected with liver diseases. However, the variables such as cigarette smoking, alcohol drinking, peanut consumption, frequent intake of raw fish, heart diseases, peptic ulcer, malaria, hypertension, diabetes, color blindness, G-6-PD deficiency, surgical operation, blood transfusion, and liver diseases of parents and children were not found to be associated with PHC.
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PMID:A case-control study of primary hepatocellular carcinoma in Taiwan. 284 88

A patient with alcoholic liver cirrhosis, diabetes mellitus and porphyria cutanea tarda (PCT) is described, who subsequently died of hepatocellular carcinoma. The literature relating PCT to the incidence of primary hepatoma is reviewed, and the mechanisms underlying this possible association are discussed.
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PMID:Is porphyria cutanea tarda a risk factor in the development of hepatocellular carcinoma? A case report and review of the literature. 298 17

Idiopathic hemochromatosis is a hereditary disease characterized by a progressive iron overload secondary to high intestinal iron absorption. After a latent period of many years, manifestations of liver cirrhosis, diabetes mellitus, cardiac failure, hypogonadism, skin hyperpigmentation and arthropathy can occur. Liver cirrhosis is the most common feature and it is complicated by hepatocellular carcinoma in 30% of cases. Tests of high sensibility are available for early diagnosis. Repeated phlebotomy can prevent clinical features in asymptomatic patients and can improve prognosis in symptomatic subjects. Current concepts in idiopathic hemochromatosis are reported in this review.
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PMID:[Idiopathic hemochromatosis]. 298 52

Insulin is thought to influence some metabolic events by decreasing the intracellular concentration of cyclic AMP (cAMP). To test whether this explains the repression of hepatic phosphoenolpyruvate carboxykinase (PEPCK) by insulin we measured intracellular cAMP, cAMP-dependent protein kinase, mRNAPEPCK, and PEPCK gene transcription in cultured Reuber H4IIE hepatoma cells treated with forskolin with and without insulin. In untreated cells, the concentration of cAMP was 2.9 pmol/mg of protein. Forskolin at 1, 10, and 50 microM increased the level of cAMP to 9.2, 35.8, and 115 pmol/mg of protein, respectively; 5 nM insulin had no significant effect on these cAMP concentrations. In untreated cells, the activity ratio of cAMP-dependent protein kinase was 0.43, and 50 microM forskolin increased this to 0.96; insulin had no effect on this ratio at times from 15-180 min. In untreated cells mRNAPEPCK bound 15 cpm of a 32P-labeled cDNA probe per microgram of total cellular RNA. Forskolin, at 1, 10, and 50 microM increased this to 48, 96, and 115 cpm/microgram RNA. Insulin (5 nM), in combination with 0, 1, 10, and 50 microM forskolin, decreased the concentration of mRNAPEPCK to 5, 8, 23, and 29 cpm/micrograms RNA, respectively. Finally, the rate of transcription of the PEPCK gene was 85, 168, 630, 823, and 884 parts per million (ppm) in H4IIE cells treated for 30 min with 0, 1, 5, 10, and 50 microM forskolin, respectively, while the corresponding rates in the presence of 5 nM insulin were 49, 45, 84, 85, and 136 ppm.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1986 May
PMID:Insulin decreases H4IIE cell PEPCK mRNA by a mechanism that does not involve cAMP. 300 46

The catabolism of low-density lipoproteins (LDL), the major cholesterol-carrying lipoproteins in plasma, is mediated in part via a high-affinity uptake pathway in the liver. Non-enzymatic glucosylation of lysine residues of apolipoprotein B, the major protein of LDL, blocks receptor-mediated uptake of LDL by fibroblasts and endothelial cells. We investigated the effect of the degree of glucosylation on the binding, uptake and degradation of radioiodinated LDL by the human hepatoma cell line Hep G2. Human LDL was glucosylated with 250 mM glucose and 30 mM cyanoborohydride at 37 degrees C. Incubations ranging from 3 to 48 h in duration resulted in the formation of 6-27% of glucitol-lysine adducts as demonstrated by coincubation with [14C]glucose. The degree of glucose incorporation corresponded to the extent of inhibition of binding, uptake and degradation of LDL (10-90%). The data are consistent with the view that glucosylation of LDL markedly impairs their catabolism. This phenomenon may be related to the pathophysiology of the premature atherosclerosis observed in diabetes mellitus.
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PMID:Impaired hepatocyte binding, uptake and degradation of glucosylated low-density lipoproteins. 301 18


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