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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Low levels of insuling stimulate transendothelial fluid transport from preswollen stroma to aqueous in rabbit corneal preparations. The rate of stromal thinning at the end of the first hour averages 30% faster with insulin, 3.5 x 10(-22) M (4.8 micromicron/ml.), than that of the paired control. This concentration is about the physiological level in rabbit aqueous. 2. The stimulation with insulin is transient. Rates of thinning average higher but not significantly different from control rates by the second hour. 3. High levels of insulin between 3.5 x 10(-9) M (480 micromicron/ml.) and 2.0 x 10(-6) M (2.75 X 10(5) micromicron/ml.) inhibit fluid transport. The inhibition at the low end of this range of concentrations becomes more pronounced with longer perfusion times but appears not to exceed ca. 50% of the control rate. 4. Ouabain also induces a biphasic effect on fluid transport which is characteristically different from that with insulin. The maximal stimulation observed at all times occurred with a fixed concentration of 10(-10) M. The stimulation is not transient but increases throughout the duration of the perfusion; the average rate is elevated 50% above the control rate by the third hour. 5. The transition from a stimulatory to an inhibitory effect occurs consistently at ca. 10(-8) M with ouabain, while a similar transition with insulin occurs at ca. 10(-9) M and appears to shift towards slightly higher concentrations during a 3 hr perfusion period. 6. Inhibition of fluid transport with ouabain, 3 x 10(-7) M, is increased from ca. 50% after 1 hr to more than 70% at the end of the third hour of perfusion. 7. The combined presence of stimulatory concentrations of ouabain and insulin affects tromal thinning in a manner resembling the effect of ouabain alone more than that of insulin; additive effects could not be discriminated. Progressively raising the concentration of insulin to a level (10(-8) M) that alone inhibits stromal thinning, ultimately abolishes the stimulatory effect of ouabain. Based on other evidence and current models of drug/hormone-membrane interaction, these results can be interpreted to indicate a concentration-dependent interaction between receptor complexes of ouabain and insulin with (Na+ + K+)-ATPase.
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PMID:Biphasic effects of insulin and ouabain on fluid transport across rabbit corneal endothelium. 63 30

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

This study defines gross, histopathologic, and radiologic changes associated with intervertebral disc degeneration in a spontaneously occurring form of the disease in aging sand rats (Psammomys obesus). Sand rats (male/female) fed lab chow supplemented with desert salt bush were sacrificed at periods of 3-30 months. Lateral thoracolumbar spine films were obtained. At sacrifice, spines were surgically exposed and gross findings were recorded; after fixation/decalcification, histopathologic studies were carried out using hematoxylin and eosin, and Safranin-O with fast green counterstain. Metabolic studies included correlations of pathologic and radiologic findings with blood glucose and insulin levels. Disc-space narrowing and subchondral endplate sclerosis increased radiologically with age, with more severe lower lumbar disc lesions. Ligamentous calcifications ventral to involved discs and caudal vertebrae were common. Disc thinning and anterior vertebral bony/cartilaginous spurs were more marked with age. Microscopy revealed loss of nucleus pulposus physaliform cells, chondrocyte replication, disc necrosis, and ossification. Hyperglycemia with and without hyperinsulinemia was common. No statistically significant differences in pathologic findings were noted, neither in diabetic versus nondiabetic nor in hyperinsulinemic animals. The sand rat is a model of disc degeneration; similarities with possible overlap with diffuse idiopathic skeletal hyperostosis syndrome were noted.
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PMID:Spondylosis in sand rats: a model of intervertebral disc degeneration and hyperostosis. 218 1

A rheological study was performed on blood samples from 10 insulin-treated diabetics with retinopathy. As part of their treatment, they all received 4 tablets of Daflon 500 mg per day for 30 days. Three complementary rheological criteria were used to characterize blood samples: 1) viscometry, using a Couette viscometer, which produces data on viscosity, shear-thinning, viscoelasticity and tixotropy of blood, 2) aggregametry, using an apparatus based on light reflectometry, using a filtrometer based on the deformations red cells undergo as they pass through narrow pores which produces information on red cell deformability. The main results were: a better red blood cell disaggregability, a decrease in red blood cell aggregation and no change in red blood cell deformability.
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PMID:Activity of Daflon 500 mg on the hemorheological disorders in diabetes. 263 48

This study reports a 22% prevalence of significant cortical osteopenia in 206 patients, aged 7-20 years, with established insulin-dependent diabetes mellitus (IDDM). A parallel decrease in trabecular bone mass was also noted. Bone loss was more evident in males (16%) than in females (6%) and was rare before 10 years of age (3%). No relationship between bone loss and the duration of diabetes, degree of metabolic control or diabetic complications was apparent. Delayed skeletal maturation did not account for cortical thinning, and the mean bone age of osteopenic diabetics was similar to that of non-osteopenic diabetics. There was no significant correlation between HLA-antigen frequency and the predisposition to diabetic osteopenia. Metabolic alterations comparable with previous findings in the chronically diabetic rat were documented in IDDM. The data documented are consistent with the conclusion that IDDM results in intestinal hyperabsorption of calcium, absorptive hypercalciuria, phosphaturia, hypomagnesaemia, hyperphosphatasaemia, and decreased circulating parathyroid hormone levels. These alterations in mineral metabolism may relate to the decrease in cortical and trabecular bone mass observed in patients with IDDM.
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PMID:Alterations of bone and mineral metabolism in diabetes mellitus. Part II. Clinical studies in 206 patients with type I diabetes mellitus. 361 83

The present study was undertaken to devise an electrophysiological method for detecting diabetic retinopathy in rats. The electroretinogram (ERG) and visual evoked potential (VEP) were recorded from unanesthetized and unrestrained rats rendered diabetic with a single i.v. injection of streptozotocin (STZ) at 35 or 40 mg/kg. The STZ-treated rats showed signs of diabetes: hyperglycemia, glucosuria, hypoinsulinemia, polyuria and increased water intake. Amplitudes of the ERG a- and b-waves and oscillatory potentials (OPs) on the b-wave were decreased and latencies of these waves were prolonged gradually after STZ was administered. Especially, latencies of the OPs became significantly different from the pre-treatment values. Latency of the VEP N1 wave showed a slight prolongation, which might be secondary to the depression of retinal function. Histological examination showed swelling and proliferation of the lens epithelium and swelling and vacuolization of the lens fiber were observed in the eyeball 9 weeks after STZ-treatment. Moreover, thinning of each retinal layer was observed in a few rats. Daily s.c. injection of insulin at 10 units/rat/day started from the 4th week. The ERG values returned to the control values after 2-3 weeks of insulin therapy. These results indicate that the ERG and VEP recording procedure used in the present study is useful for early detection of the diabetic retinopathy in rats and that the OP of the ERG appears to be vulnerable to diabetes in the rat as it is in the human.
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PMID:[An electrophysiological method for detecting diabetic retinopathy in rats]. 639 51

20 puncture renal biopsies and 16 pancreatic biopsies from patients with insulin-dependent diabetes mellitus were studied ultrastructurally. The stages in the development of kidney changes depending on the functional state of Langerhans islands B-cells were established. The 1st stage includes signs of segmentary mesangioproliferative glomerulonephritis- segmentary increase of the mesangium due to the hypercellularity, variability of the basal membrane thickness in the glomeruli capillaries, leucocytes in the lumen, subendothelial deposits. This stage may be due to the persistence of the etiologic factors(virus), formation of circulating immune complexes, antibodies excess and relative preservation of B-cells and their function. Thinning of the capillary basal membrane, decrease of the mesangial matrix surface, cell destruction are characteristic for the 2nd stage- stage of the mesangiolysis. The duration of disease up to 15 years has no influence on the formation of glomerulosclerosis.
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PMID:[Diabetic glomerulonephritis--the first stage of diabetic glomerulopathy]. 784 5

Streptozotocin diabetic rats showed an increase of bone fragility (11.9 +/- 2.1 kg/cm2 vs. 16.8 +/- 2.0, P < 0.005) which was normalized by insulin treatment (18.3 +/- 4.2), indicating that osteoporosis was induced in diabetic rats. The rats were fed a zinc-deficient diet (0.16 mg/100 g) or a control diet (5.2 mg/100 g). This mild zinc-deficient diet did not lower the serum zinc level. The cortical bone of diabetic rats was shown to be markedly thinner by microscopic examination of ground cross-sections of the tibia. Zinc deficiency induced a reduction in the calcium content of diabetic bone when compared with the rats on a control diet. Urinary excretion of calcium and phosphorus was significantly increased in diabetic rats, and increased further when the rats were fed a zinc-deficient diet. Moreover. the bone calcium and phosphorus concentrations were significantly lower in these animals. These changes in the zinc-deficiency rats were not reversed by insulin treatment. Our findings suggest that osteoporosis in the diabetic rats was due to thinning of the bone cortex secondary to mineral loss and can be reversed by insulin treatment, and that these skeletal changes are greatly enhanced by mild zinc deficiency. In addition the effects of zinc deficiency cannot be completely reversed by insulin treatment.
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PMID:Zinc deficiency exaggerates diabetic osteoporosis. 840 52

In three patients, a 36-year-old HIV seropositive homosexual man and two women aged 35 and 59 years who had acquired HIV infection through heterosexual contact, signs of lipodystrophy developed after prolonged anti-HIV triple therapy. The observed syndrome is seen after prolonged use of HIV protease inhibitors: it is characterized by peripheral fat wasting, central fat accumulation, hyperlipidaemia and insulin resistance. Typically the subcutaneous fatty tissue disappears resulting in prominent zygomata, veins and muscles and thinning of extremities and buttocks. In addition to abdominal fat accumulation, there have been reports on the occurrence of a dorsocervical fat pad, the so-called buffalo hump. Lipodystrophy caused by protease inhibitors is a risk factor for cardiovascular disease. Recognition of the syndrome is essential for adequate follow-up and possible treatment.
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PMID:[Lipodystrophy and 'buffalo hump' during treatment with HIV protease inhibitors]. 1006 60

Growth retardation in children with thalassaemia major is multifactorial. We studied the growth hormone (GH) response to provocation by clonidine and glucagon, measured the circulating concentrations of insulin, insulin-like growth factor-I (IGF-I), IGF-binding protein-3 (IGFBP3), and ferritin, and evaluated the spontaneous nocturnal (12 h) GH secretion in prepubertal patients with thalassaemia and age-matched children with constitutional short stature (CSS) (height SDS < -2, but normal GH response to provocation). The anatomy of the hypothalamic pituitary area was studied in patients with abnormal GH secretion using MRI scanning. Children with thalassaemia had significantly lower peak GH response to provocation by clonidine and glucagon (8.8 +/- 2.3 micrograms/l and 8.2 +/- 3.1 micrograms/l respectively) than did controls (17.6 +/- 2.7 micrograms/l and 15.7 +/- 3.7 micrograms/l respectively). They had significantly decreased circulating concentrations of IGF-I and IGFBP3 (68.5 +/- 19 ng/ml and 1.22 +/- 0.27 mg/l respectively) compared to controls (153 +/- 42 ng/ml and 2.16 +/- 0.37 mg/l respectively). Seven of the thalassaemic children had a GH peak response of < 7 micrograms/l after provocation. Those with a normal GH response after provocation also had significantly lower IGF-I and IGFBP3 concentrations than controls. Analysis of their spontaneous nocturnal GH secretion revealed lower mean (2.9 +/- 1.77 micrograms/l) and integrated (2.53 +/- 1.6 micrograms/l) concentrations compared to controls (4.9 +/- 0.29 micrograms/l and 5.6 +/- 0.52 micrograms/l respectively). Five of them had mean nocturnal GH concentration < 2 micrograms/l and four had maximum nocturnal peak below 10 micrograms/l. These data denoted defective spontaneous GH secretion in some of these patients. MRI studies revealed complete empty sella (n = 2), marked diminution of the pituitary size (n = 4), thinning of the pituitary stalk (n = 3) with its posterior displacement (n = 2), and evidence of iron deposition in the pituitary gland and midbrain (n = 7) in those patients with defective GH secretion (n = 9). Serum ferritin concentration was correlated significantly with the circulating IGF-I (r = -0.47, p < 0.01) and IGFBP3 (r = -0.43, p < 0.01) concentrations. These data prove a high prevalence of defective GH secretion in thalassaemic children associated with structural abnormality of their pituitary gland.
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PMID:Spontaneous and provoked growth hormone (GH) secretion and insulin-like growth factor I (IGF-I) concentration in patients with beta thalassaemia and delayed growth. 1066 1


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