[Severe poisoning with thyroid hormones in a body builder].
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Adolescent↗
Biomedical subjects
B Richelsen
Publications and source records attributed to B Richelsen.
Increased insulin binding to adipocytes and monocytes and increased insulin sensitivity of glucose transport and metabolism in adipocytes from non-insulin-dependent diabetics after a low-fat/high-starch/high-fiber diet.
Nine non-insulin-dependent diabetics were studied before and after 3 weeks on an isoenergetic high-fiber/high-starch/low-fat diet (alternative diet), and nine non-insulin-dependent diabetics were studied on their usual diet. In the group that ate the alternative diet, the intake of fiber and starch increased 120% and 53%, whereas fat intake decreased 31%. Diabetes control improved as demonstrated by decreased fasting plasma glucose (P less than 0.05) and 24-hour urinary glucose excretion (P less than 0.05). The in vivo insulin action increased (KIVITT increased, P less than 0.05) with no change in fasting serum insulin levels. In fat cells obtained from patients in the alternative-diet group, insulin receptor binding increased (P less than 0.05) after the change of diet. Insulin binding to purified monocytes (more than 95% monocytes) also increased (P less than 0.05), whereas no change was found in insulin binding to erythrocytes. When lipogenesis was studied at a tracer glucose concentration at which glucose transport seems to be rate limiting, insulin sensitivity increased (P less than 0.02). This is the predicted consequence of increased receptor binding. Moreover, when CO2 production and lipogenesis were studied at a higher glucose concentration, where steps beyond transport seem to be rate limiting for glucose metabolism, increased insulin sensitivity was also observed. In contrast, no change was found in maximal insulin responsiveness. Fat and blood cells from the patients who continued on their usual diet showed no changes of the mentioned quantities.(ABSTRACT TRUNCATED AT 250 WORDS)
Adipose Tissue↗
Antral gland cell column: a method for studying release of gastric hormones.
A technique for studying in vitro release of gastric hormones has been developed. The system utilizes nonenzymatically isolated antropyloric glands from humans or rats, which are perifused in a Bio-Gel P-2 column. The system permits the study of kinetics and dose-response characteristics using the glands as their own control. The glands were stimulated with carbachol and bombesin, and the antral peptides gastrin and somatostatin were measured. Bombesin and carbachol both evoked a dose-dependent stimulation of gastrin release, beginning at below 10(-10) M (bombesin) and 10(-7) M (carbachol). Carbachol inhibited the release of somatostatin in a dose-dependent manner, being maximally effective at 10(-6) M and then producing 60% inhibition of somatostatin release. Bombesin was without effect on antropyloric somatostatin release. These data suggest that the gastrin-stimulating effect of carbachol is partially or totally due to inhibition of somatostatin release, whereas bombesinergic stimulation of gastrin release must work in an independent manner. In addition, data on the effects of these substances on the release of gastrin and ACTH-like peptides from human antropyloric glands are presented. Due to the absence of local neural reflexes, this system is a useful supplement to the isolated perfused stomach model.
Acetylcholine↗
The effect of glibenclamide on insulin receptors in normal man: comparative studies of insulin binding to monocytes and erythrocytes.
In vivo studies in noninsulin-dependent diabetic patients have indicated that sulphonylurea drugs have an extra-pancreatic effect. To further elucidate the mechanisms of this action, we studied the effect of glibenclamide on in vivo and in vitro cellular insulin receptor binding in normal subjects. Oral administration of glibenclamide in dose of 2.5 mg/day increased insulin binding to monocytes by 70% (P less than 0.001), in spite of increased postprandial serum insulin levels. This change in insulin receptor binding occurred in the absence of changes in diet or body weight. In contrast, glibenclamide had no stimulatory effect on in vivo insulin binding to erythrocytes. The in vitro studies with monocytes revealed a dose-related insulin receptor stimulatory effect of glibenclamide (P less than 0.05), with a maximal effect of 20% above basal level. These data indicate that glibenclamide increases the insulin-binding ability of monocytes but not of erythrocytes. As the monocyte is judged a better model for studying insulin receptors on target cells than the erythrocyte, this effect may be responsible, at least in part, for the extrapancreatic effect of sulphonylureas, which seem to be of major importance for their hypoglycemic effect in noninsulin-dependent diabetic patients.
Blood Glucose↗
[Social and medical indicators for prognosis and case-closure status at a rehabilitation clinic].
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Adolescent↗
Increased insulin binding is not involved in the improved insulin effectiveness of gestational diabetics after hypoenergetic dieting.
125I-Insulin binding to monocytes from 14 gestational diabetics was measured before and after 6 weeks of treatment with a 5500 kJ, low-fat, low-sucrose diet. After the hypoenergetic feeding of gestational diabetics, fasting plasma concentrations of glucose (P less than 0.01) and insulin (P less than 0.05) decreased significantly, whereas insulin binding was unaltered. Provided the monocyte insulin receptor reflects insulin receptors of more determinant tissues for insulin action, our data indicate that an increased insulin receptor binding is not involved in the improved insulin effectiveness of gestational diabetics after hypoenergetic dieting.
Adult↗
Regulation of plasminogen activitor inhibitor-1 in human adipose tissue: interaction between cytokines, cortisol and estrogen.
To investigate further the role of plasminogen activator inhibitor-1 (PAI-1) in human adipose tissue, the regulation of cytokines, cortisol (dexamethasone) as well as estrogen on PAI-1 were determined in human adipose tissue fragments. PAI-1 activity was increased in human adipose tissue fragments incubated for 48 h with interleukin-1beta (IL-1beta) (2.6-fold, p < 0.01) and tumor necrosis factor-alpha (2.3-fold, p < 0.01). Incubation with interleukin-6 revealed a non-significant decrease in PAI-1 activity. Parallel findings were obtained when studying the PAI-1 mRNA expression. Dexamethesone increased PAI-1 activity after incubation for 8 h (p < 0.05) and enhanced the stimulation of IL-1beta after 8 h incubation. However, after 24 and 48 h, dexamethasone significantly reduced the IL-1beta induced increase in PAI-1 activity by 24-52% (p < 0.05), accordingly, PAI-1 mRNA expression was reduced 60%. Finally, the induction of PAI-1 activity and PAI-1 mRNA expression by IL-1beta was attenuated by estrogen (17.8+/-4.9%, p < 0.05 and 20.9+/-5.8%, p < 0.05, respectively). These results indicate that multiple cytokines, estrogen and dexamethasone may be involved in the regulation of PAI-1 biosynthesis in human adipose tissue, and suggest that there are interactions between cytokines and these steroid hormones. The interplay between these hormones may be of importance for the levels of PAI-1 observed in obesity and associated states.
Adipose Tissue↗
Interleukin-8 production in human adipose tissue. inhibitory effects of anti-diabetic compounds, the thiazolidinedione ciglitazone and the biguanide metformin.
Obesity and Type 2 diabetes are associated with an increased risk of developing cardiovascular disease. Reports have suggested that the chemokine, interleukin-8, may be involved in the development of diabetic macroangiopathy as well as in the pathogenesis of atherosclerosis. Two classes of drugs, the biguanides and the insulin-sensitizing thiazolidinediones seem to have additional beneficial effects on cardiovascular risk-factors besides their effects on glucose homeostasis. In this study, we investigated the effects of the thiazolidinedione, Ciglitazone, the peroxisome proliferator-activated receptor alpha-agonist 5,8,11,14-eicosatetraynoic acid (ETYA) and the biguanide, Metformin on interleukin-8 gene expression and production in human adipose tissue in vitro. Ciglitazone 10-100 M inhibited interleukin-8 release by 25-33% (p < 0.05) and mRNA expression by 33-60% (p < 0.05). Metformin 0.1-10 mM inhibited interleukin-8 release by 20-50% (p < 0.05) and mRNA expression by 20-90% (p < 0.05). However, ETYA did not effect the production of interleukin-8 in the adipose tissue. In conclusion, we demonstrate the ability of two anti-diabetic compounds to decrease the release of interleukin-8 from human adipose tissue in vitro. These findings open the possibility that the beneficial effects on cardiovascular risk-factors of these anti-diabetic compounds might involve a reduction in the interleukin-8 produced in human adipose tissue.
5,8,11,14-Eicosatetraynoic Acid↗
Effect of insulin pump treatment for one year on renal function and retinal morphology in patients with IDDM.
The effect of strict metabolic control for 1 yr on renal function and retinal morphology was estimated in 24 insulin-dependent diabetic individuals (age 29 +/- 8 yr, diabetes duration 10 +/- 6 yr) with Albustix negative urine and minimal or no background retinopathy before the study. They were randomized to conventional insulin treatment (CIT) or continuous subcutaneous insulin infusion (CSII) with a portable pump. During CSII treatment the metabolic status was significantly improved and glomerular filtration rates (GFR) were found to decline (from 130 +/- 18 to 116 +/- 15 ml/min/1.73 m2, P less than 0.01). The mean value of urinary albumin excretion (UAE) was not statistically significantly reduced (from 15.3 +/- 24.1 to 6.8 +/- 1.5 mg/24 h, P greater than 0.1). In the CIT group both GFR and UAE values were unchanged. In all subjects before treatment we found a positive correlation between the metabolic status, estimated by the HbA1c values, and GFR as well as UAE values, respectively (r = 0.64, P less than 0.01 and r = 0.42, P less than 0.05). We conclude that elevated GFR values can be reduced toward normal level by insulin pump treatment for 1 yr. Retinal morphology was found to deteriorate in four of 12 CIT subjects and in three of 12 CSII subjects. However, the progression was mild and in most individuals only due to a slight increase in the number of microaneurysms. Pump treatment did not induce proliferation and "cotton-wool" exudates were not detectable in any pump subject after 1 yr of treatment. We conclude that CSII treatment for 1 yr was unable to stop the progression of retinopathy in individuals with minimal or no retinopathy on entering the study. On the other hand, pump treatment did not induce cotton-wool exudates or proliferation in these subjects as previously reported in subjects with more severe retinopathy before CSII treatment.
Adult↗
Sulfonylureas improve insulin binding and insulin action in non-insulin-dependent diabetes mellitus.
Sulfonylureas reduce plasma glucose concentrations in most patients with non-insulin-dependent diabetes mellitus (NIDDM). The mechanism of this action is controversial. In this article we examine the issue of the peripheral effect of these drugs, i.e., the effect on insulin receptors and insulin action. In our studies we have found that sulfonylureas possess a selective regulatory in vivo effect on the cellular insulin binding to monocytes, independent of the diet and changes in plasma glucose and insulin concentrations. Furthermore, we found in in vitro studies that sulfonylureas affect the insulin receptors in a direct way. Thus, insulin binding to monocytes was increased during sulfonylurea treatment in both normal volunteers and patients with NIDDM. On the other hand, sulfonylureas seem to improve insulin action in NIDDM patients only. We conclude that the increased insulin binding in patients with NIDDM, induced by sulfonylurea treatment, may be of importance for the improved insulin action found in these patients. However, this hypothesis has to be proved.
Binding, Competitive↗