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

The effects of long-term high-fiber diet on lipid and glucose levels and the histological changes in the coronary arteries and thoracic aorta in STZ-induced diabetic SD rats were investigated. During the first 4 weeks of the study period, all diabetic rats were given regular chow plus water after which, all were grouped according to the following diet regimen: group II, no added cholesterol and glucomannan; group III, no added cholesterol but with glucomannan supplement, group IV, with added cholesterol but no glucomannan supplement; and group V, with both cholesterol and glucomannan supplements. 15% weight of glucomannan and 1.5% weight of cholesterol in regular rat chow were used as supplements when indicated. Non-diabetic rats which received only regular chow served as the control group (group I). In the 18th week all rats were sacrificed and weight gain, glucose, total cholesterol, HDL-cholesterol, triglyceride and lipid peroxidase concentrations were determined. Selected portions of the heart and thoracic aorta were histologically examined. Weight gain was higher in rats supplemented with glucomannan than in those without glucomannan supplements, but the difference is not significant. A lowering tendency in glucose levels was likewise observed. Furthermore, total cholesterol and HDL-cholesterol levels were lower and higher, respectively in diabetic rats receiving glucomannan. Although the triglyceride levels were similar in all rats, lipid peroxidase levels were significantly lower in rats with high-fiber diet.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1991 Sep
PMID:Effects of long-term high-fiber diet on macrovascular changes and lipid and glucose levels in STZ-induced diabetic SD rats. 165 79

Insulin receptor tyrosine kinase activity solubilized from hind limb muscle of control and streptozocin-induced diabetic (STZ-D) rats (2-3 wk) was studied with the substrates histone H2B and poly glutamic acid-tyrosine (glu-tyr) (4:1). Basal and insulin-stimulated kinase activities were inhibited when high concentrations of either substrate were added before initiation of phosphorylation with ATP. Under these conditions, insulin-stimulated activities of diabetic- and control-derived receptor kinase toward H2B were similar at 0.008 mg/ml H2B. However, higher concentrations of H2B (0.04-1 mg/ml) progressively reduced the ratios of diabetic-derived to control-derived receptor kinase activities to approximately 0.5. When inhibition of receptor kinase activities was prevented by allowing maximal autophosphorylation of insulin receptors before addition of H2B, kinase activity of diabetic- and control-derived receptors was similar at all H2B concentrations. Diabetic-derived insulin-receptor tyrosine kinase activity toward poly glu-tyr (4:1) was not significantly different from that of control rats. Under conditions of substrate inhibition (0.4 mg/ml H2B), insulin receptor H2B kinase activity from muscles of rats with severe diabetes (85 mg/kg STZ, 7 days) was significantly decreased, whereas the same activity from rats with moderate diabetes (50 mg/kg STZ, 7 days) was not significantly different from control rats. Insulin receptor alpha,beta dimers were not detectable in muscle preparations from control or diabetic rats. The data suggest that the impairment of muscle-derived insulin-receptor tyrosine kinase activity associated with insulinopenic diabetes reflects, in part, enhanced inhibition by some substrates. If solubilized insulin receptors and the exogenous substrates studied model in vivo events, impaired signaling of the muscle insulin receptor in insulinopenic diabetes may depend on the type and concentration of intracellular tyrosine kinase substrates and the severity of the metabolic derangements.
Diabetes 1991 Dec
PMID:Skeletal muscle insulin-receptor kinase. Effects of substrate inhibition and diabetes. 166 94

The influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone (T) and hypothalamic neurotransmitter turnover rates in adult male rats was evaluated. Adult male Sprague-Dawley rats were made diabetic by an intraperitoneal injection of streptozotocin (STZ; 5 mg/100 g body weight) in citrate buffer. Vehicle-injected rats served as controls. On day 9, all rats were bilaterally castrated and treated subcutaneously on alternate days with either peanut oil or T propionate (TP) in peanut oil (100 micrograms/rat). Plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), and T concentrations were measured by specific radioimmunoassays from blood samples collected on day 1 (before castration) and 2, 4, 6, and 7 days after castration. On day 7 after castration (day 15 after vehicle or STZ treatment), 1 h before autopsy, the rats were injected intraperitoneally with saline or a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine (25 mg/100 g BW), for the measurement of norepinephrine (NE) and dopamine turnover in median eminence and medial basal hypothalamus (MBH). Circulating FSH, LH, PRL, and T levels were significantly lower (FSH and T: p less than 0.001; LH and PRL: p less than 0.05) in gonad-intact rats treated with STZ than in vehicle-injected animals. The castration-induced increase in plasma LH levels was attenuated in diabetic rats. The suppressive effect of T on LH secretion was significantly greater (p less than 0.001) in STZ-treated rats relative to TP-treated nondiabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone and hypothalamic neurotransmitter turnover in adult male rats. 168 39

Insulin responses to nutrient secretagogues were investigated in neonatally streptozotocin-injected (n-STZ) rats, i.e. an animal model of noninsulin-dependent diabetes. In the perfused pancreas 16 mM L-glutamine induced and 10 mM octanoate tended to induce (P less than 0.2) higher responses in n-STZ than in nondiabetic rats. Addition of 3.9 mM glucose potentiated responses to glutamine and octanoate more in n-STZ (3.3- and 3.4-fold) than in nondiabetic rats (1.5- and 1.9-fold). Conversely, the succinate derivative succinate monomethylester (Succ ME) induced lesser response in n-STZ rats (57% of that in nondiabetic rats) and coperfusion with 3.9 mM glucose increased the response less in n-STZ (1.4-fold) than in nondiabetic rats (3.8-fold). Pyruvate (20 mM) mimicked the potency of 3.9 mM glucose, i.e. pyruvate potentiated the response to Succ ME only nonsignificantly (1.2-fold) in n-STZ but markedly (4.9-fold) in nondiabetic rats. Dichloroacetate (20 mM) failed to affect the response to Succ ME together with pyruvate in n-STZ rats. To investigate the role of hyperglycemia for octanoate-induced secretion, nondiabetic rats were made hyperglycemic by 48-h glucose infusions. Octanoate-induced secretion from perfused pancreas was enhanced 3.8-fold after moderate hyperglycemia (13.2 +/- 0.6 mM) and 17-fold after marked hyperglycemia (22.7 +/- 0.6 mM). This positive association between response and degree of hyperglycemia was not found with a nonnutrient secretagogue, 3-isobutyl-1-methylxanthine. Results with glutamine and octanoate indicate that oxidation of nonglucose nutrients which normally do not regulate secretion is enhanced secondary to chronic hyperglycemia. Results with Succ ME and pyruvate suggest that early steps of oxidation of glucose are impaired in n-STZ rats.
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PMID:Multiple abnormalities in insulin responses to nonglucose nutrients in neonatally streptozotocin diabetic rats. 170 69

Abnormalities in axonal transport have been observed in human and experimental diabetes and may be related to the pathogenesis of diabetic neuropathy. Axonal transport has previously been evaluated by indirect methods. In this study, direct-measurement techniques were applied (with computer-enhanced video-recorded images) for the first time to evaluate intra-axonal organelle speed and frequency (the amount of organelle traffic) in both the anterograde fast component (AFC) and retrograde fast component (RFC) of axonal transport in diabetic nerve. Sciatic nerve and dorsal and ventral nerve roots were studied in the animal model of insulin-dependent diabetes (BB/Wistar rat) and sciatic nerve in the non-insulin-dependent (streptozocin-induced) model of diabetes (STZ-D rat). STZ-D rats were studied at 1 mo, and BB/Wistar rats were studied at 1 and 2 mo of diabetes duration. Statistically significant decreases in peripheral axon organelle speed were found only for RFC at 1 mo of diabetes in both the BB/Wistar (8.1%) and STZ-D (5.4%) rats. The difference was no longer significant in BB/Wistar rats at 2 mo of diabetes. This recovery suggests that the underlying abnormality is reversible. No differences were seen in AFC of any axons, and the only other difference seen was a 5.1% decrement in RFC at 2 mo in the ventral roots. No significant difference was observed in any group for organelle frequencies. Other factors should be considered to explain the decrease in materials transported in accumulation studies. The transient deficits in RFC speed observed remain of undetermined significance in the pathogenesis of diabetic neuropathy.
Diabetes 1991 Jan
PMID:Amount and speed of fast axonal transport in diabetes. 170 37

1. Adult male Wistar rats were injected with streptozotocin (STZ: 55 mg/kg) for inducing diabetes. Then blood and atria for RNA extraction were withdrawn from rats treated 3 and 11 weeks previously with STZ respectively. Atrial total RNA were extracted with cold phenol method. The ANP mRNA contents were determined using Dot blot hybridization technique with alpha-32-P-labelled r-prepro ANP cDNA probe. 2. Plasma glucose was increased and plasma immunoreactive insulin was lowered in rats at 3 and 11 weeks after injection of STZ. ANP gene expression in diabetic rats was depressed. ANP mRNA contents in rats treated 3 and 11 weeks with STZ were 86.4% and 31.7% of that of control rats. 3. Three weeks after treatment of STZ, the rats were gastrically perfused with FOC (Fish Oil Compound) (0.355 ml/kg) once a day successively until 11 weeks. This treatment induces lower blood pressure in rats. ANP gene expression in FOC group was apparently recovered which had been decreased because of the effect of diabetes mellitus.
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PMID:The effects of streptozotocin induced diabetes mellitus and fish oil compound on gene expression of atrial natriuretic peptide in rat. 171 56

The fast and slow components of the mechanical response to 1 microM norepinephrine (NE) were measured in aortic rings isolated from eight spontaneously diabetic rats, six streptozocin-induced diabetic (STZ-D) rats, six STZ-D rats treated with 2.5 U insulin/day during the 4 days before being killed, and six age- and sex-matched control rats. The total contraction to NE (i.e., the sum of fast and slow components) was similar in the four groups: spontaneously diabetic, 16.53 +/- 1.72 mN; STZ-D, 15.68 +/- 1.41 mN; insulin-treated, 16.17 +/- 2.05 mN; and control, 15.27 +/- 0.96 mN (NS). The fast component, measured graphically in a total contraction in 1.35 mM Ca, was greater in spontaneously diabetic (12.61 +/- 1.07 mN, P less than 0.05) and STZ-D (12.25 +/- 0.89 mN, P less than 0.05) rats compared with control (9.14 +/- 0.74 mN) or insulin-treated (8.58 +/- 1.23 mN) rats. The same increase of the fast component was detectable after 3 min of incubation in Ca-free medium + 2 mM EGTA (control 6.54 +/- 0.47 mN, spontaneously diabetic 9.07 +/- 0.76 mN, P less than 0.05; STZ-D 8.82 +/- 0.72 mN, P less than 0.05), and it was also abolished by insulin treatment (insulin-treated 6.29 +/- 0.36 mN). We conclude that the diabetic state increases the fast component of NE-induced contraction either in the absence or presence of Ca in the medium. This suggests that such an increase depends on a larger release of Ca from intracellular stores.
Diabetes 1992 Jan
PMID:Effect of diabetes on fast response to norepinephrine in rat aorta. 172 36

Autonomic neuropathy is a common complication of diabetes. In this study we evaluated autonomic neuropathy by determining somatostatin (S-14)-evoked acetylcholine (Ach) release from postsynaptic parasympathetic fibers in the atria of controls (C) and streptozotocin diabetic rats (STZ-D), with and without tetrodotoxin (TTX). The release induced by S-14 did not differ in C and STZ-D. TTX blocked S-14 induced Ach in C but failed in STZ-D. TTX resistance in STZ-D may be explained by variations of membrane potential in nerve fibers.
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PMID:Acetylcholine release in experimental autonomic neuropathy. 174 33

Streptozocin-induced diabetic (STZ-D) mice have reduced brain concentrations of tryptophan, a precursor substance for 5-hydroxytryptamine, and show lengthened immobility in Porsolt's swim test, a putative animal model of depression. This study investigated whether tryptophan affects behavior in Porsolt's swim test in STZ-administered male National Institutes of Health Swiss mice. In addition, the effect of tryptophan on behavior in the resident-intruder test of aggression was studied. Tryptophan is effective in the treatment of mild depression and may reduce aggressive behavior. Diabetes was induced with injection of 200 mg/kg body wt i.p. STZ. Two weeks after STZ treatment, the mice received 0, 50, and 100 mg/kg i.p. tryptophan 60 min before the swim test. The STZ-administered mice exhibited lengthened immobility in the swim test, and tryptophan caused a dose-related shortening in their immobility times. The control and STZ mice, which were isolated for 1 wk before the resident-intruder test, did not show any difference in the time spent in social investigation or aggressive or defensive behaviors. However, 100 mg/kg i.p. tryptophan 60 min before the test reduced the social interaction and aggressive behavior of the STZ-D mice but increased these behaviors in controls. Results indicate that tryptophan shortens the increased immobility time and reduces social and aggressive behavior in STZ-D mice. Therefore, the reported reductions in the brain-tryptophan concentrations in STZ-D mice may participate in regulating their behavior.
Diabetes 1991 Dec
PMID:Effects of tryptophan on depression and aggression in STZ-D mice. 175

Quantitative light and electronmicroscopical morphometric techniques were used to determine the effect of pancreatic islet transplantation on experimental diabetic neuropathy. Groups of STZ-diabetic rats were given islet transplants at 3 weeks after diabetes onset (prevention) and at 6 months after diabetes onset (reversal). Comparisons were made with onset controls, age-matched non-diabetic controls and untreated diabetic controls 6 months later (n = 8 for all groups). Euglycaemia and normal levels of glycosylated haemoglobin were achieved in both groups of diabetics after islet transplantation. Loss of body weight in diabetic animals was prevented by early islet transplantation, but was only partially reversed following delayed islet transplantation. Normal growth of myelinated fibres and axons during development was retarded in untreated diabetics, but was normal in rats given islet transplants soon after the onset of diabetes (cross-sectional perimeter and area). Diabetics transplanted with islets after a delay had myelinated fibres and axons with diminished calibre. Teased fibre preparations of nerves from diabetics which had received islet transplants showed no excess of abnormalities. This study has shown that the development of certain structural abnormalities of peripheral nerve fibres is prevented in diabetic rats which receive transplants of islets of Langerhans soon after the onset of diabetes. However, once established abnormal fibre morphology can not be completely ameliorated merely by achieving and sustaining euglycaemia through delayed islet transplantation.
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PMID:The effect of pancreatic islet transplantation on experimental diabetic neuropathy. 175 93


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