Biomechanical changes in connective tissues induced by experimental diabetes

1981 ◽  
Vol 98 (3) ◽  
pp. 432-436 ◽  
Author(s):  
T. T. Andreassen ◽  
K. Seyer-Hansen ◽  
H. Oxlund
Keyword(s):  
Maximum Stress ◽  
Insulin Treatment ◽  
Experimental Diabetes ◽  
Biomechanical Testing ◽  
Streptozotocin Diabetes ◽  
Biomechanical Properties ◽  
Diabetic Rats ◽  
Collagen Content ◽  
Connective Tissues ◽  
Biomechanical Changes

Abstract. The biomechanical properties of skin and aorta were studied in rats with experimental (streptozotocin) diabetes. After 30 days of diabetes the collagen content of the skin was diminished by 30%. By biomechanical testing collagen from diabetic rats was found to exhibit increased stiffness and strength: maximal stiffness was increased by 20% and the strain at maximum stress was decreased by 10%. Insulin treatment prevented all changes. No differences were found between aortic specimens from diabetic and normal rats.

Chondrosarcoma growth: influence of diabetes, caloric restriction, and insulin treatment

1981 ◽  
Vol 241 (2) ◽  
pp. E129-E135 ◽  
Author(s):  
W. D. McCumbee ◽  
H. E. Lebovitz
Keyword(s):  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Diet Restriction ◽  
Cartilage Growth ◽  
Serum Pool ◽  
In Vivo Growth

Diabetes and malnutrition result in decreased somatomedin production and cartilage growth in rats. The growth and metabolism of the Swarm rat chondrosarcoma are dramatically affected by somatomedins. Data presented here show that streptozotocin diabetes and diet restriction inhibit in vivo chondrosarcoma growth. Tumors grown in diabetic rats were significantly smaller than tumors grown in diet-restricted rats showing the same changes in body weight. Insulin treatment increased the rate of tumor growth in diabetic rats. Tumors grown in rigidly controlled diabetic rats were as large as tumors grown in nondiabetic controls. Diet restriction and diabetes reduced the capacity of the serum of the rat to stimulate alpha-amino[14C]isobutyrate uptake and [3H]uridine incorporation into RNA in chondrosarcoma pieces grown in nondiabetic rats. This somatomedin activity of the serum was restored by treating diabetic rats with insulin. There was a significant correlation between the in vitro stimulatory effect of a particular serum pool on chondrosarcoma metabolism and in vivo chondrosarcoma growth in the animals from whom the serum was obtained. These studies demonstrate that the in vivo growth of malignant chondrocytes is similar to that of normal chondrocytes with respect to the role of nutrition and insulin.

scholarly journals Factors influencing the altered thermogenic response of rat brown adipose tissue in streptozotocin-diabetes

1988 ◽  
Vol 249 (2) ◽  
pp. 415-421 ◽  
Author(s):  
Z Jamal ◽  
E D Saggerson
Keyword(s):  
Blood Flow ◽  
Maximum Rate ◽  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Brown Fat ◽  
Male Rats ◽  
Maximum Effect ◽  
O2 Uptake ◽  
Flow Through

1. Adipocytes were isolated from the interscapular brown fat of male rats maintained at 21 degrees C. These animals were controls, streptozotocin-diabetics or 2-day insulin-treated diabetics. 2. With adipocytes from diabetic animals, maximum rates of noradrenaline-stimulated O2 uptake were decreased by 58%, and the Bmax. of [3H]GDP binding to mitochondria was decreased by 55%. Insulin administration reversed both of these changes. 3. Streptozotocin-diabetes increased basal lipolysis in adipocytes incubated with adenosine deaminase (1 unit/ml), decreased the EC50 (concn. giving 50% of maximum effect) for noradrenaline, but did not change the maximum rate of noradrenaline-stimulated lipolysis. Except for some small differences at very low concentrations (10-100 pM), diabetes or insulin treatment did not alter the sensitivity of noradrenaline-stimulated lipolysis or O2 uptake to the inhibitory effect of N6-phenylisopropyladenosine. It is therefore concluded that the lesion(s) in thermogenesis in diabetes are not attributable to any changes in lipolysis. 4. Blood flow through interscapular brown fat, measured by accumulation of [14C]DDT [14C-labelled 1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane] was increased by 2.3-fold 70 min after a single administration of insulin to diabetic rats. This treatment decreased blood flow through epididymal white fat by 58%. 5. Propranolol treatment of diabetic rats muted the ability of insulin treatment to increase the maximum rate of noradrenaline-stimulated O2 uptake, suggesting that this action of insulin may be a secondary one rather than a direct effect of the hormone on the adipocytes.

scholarly journals Effects of streptozotocin-diabetes and insulin administration in vivo or in vitro on the activities of five enzymes in the adipose-tissue triacylglycerol-synthesis pathway

1987 ◽  
Vol 243 (1) ◽  
pp. 289-292 ◽  
Author(s):  
E D Saggerson ◽  
C A Carpenter
Keyword(s):  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diacylglycerol Acyltransferase ◽  
Fatty Acyl ◽  
Diabetic Rats ◽  
Insulin Administration ◽  
Triacylglycerol Synthesis ◽  
Phosphatidate Phosphohydrolase

At 2 days after administration of streptozotocin (100 mg/kg), activities in rat epididymal fat-pads of the following enzymes were significantly decreased: fatty acyl-CoA synthetase (FAS), mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), monoacylglycerolphosphate acyltransferase (MGPAT) and Mg2+-dependent phosphatidate phosphohydrolase (PPH). There were no significant changes in diacylglycerol acyltransferase or Mg2+-independent PPH. Insulin administration to diabetic rats over 2 days restored activities of FAS, both forms of GPAT, MGPAT and Mg2+-dependent PPH. Significant restoration of all five activities was also seen 2 h after a single administration of insulin, but was not observed 45 min after insulin treatment. Insulin significantly increased all five enzyme activities when adipocytes from diabetic rats were incubated for 2 h with a mixture of glucose, lactate, pyruvate and amino acids.

Effects of diabetes on oxidative decarboxylation of branched-chain keto acids

1980 ◽  
Vol 239 (3) ◽  
pp. E215-E222 ◽  
Author(s):  
M. E. May ◽  
V. J. Mancusi ◽  
R. P. Aftring ◽  
M. G. Buse
Keyword(s):  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Relative Increase ◽  
Oxidative Decarboxylation ◽  
Decarboxylase Activity ◽  
Mitochondrial Mass ◽  
Keto Acids ◽  
Branched Chain ◽  
Ketoacid Dehydrogenase

Oxidative decarboxylation is the first irreversible step in the degradation of leucine. The effect of streptozotocin diabetes on this reaction was studied in cell-free rat liver preparations, using [1-14C]alpha-ketoisocaproate as substrate. Diabetes increased the branched-chain ketoacid dehydrogenase (BCKD) activity (per g liver or per mg protein) of homogenates, but the ratios of homogenate BCKD activity to other mitochondrial markers remained unchanged. A cytosolic branched-chain ketoacid decarboxylase activity (15-22% of homogenate activity), which did not require NAD, CoA, or NADP, was also increased in diabetics. Insulin treatment of diabetics normalized enzyme activity in all fractions. The apparent Km of BCKD in homogenates was 43-45 microM; diabetes increased the apparent Vmax from 165 nmol x min-1 x g tissue-1 to 260 nmol x min-1 x g-1. In contrast, the Km for cytosolic alpha-ketoisocaproate decarboxylation was 270 microM in controls, and diabetes resulted in both a lower Km (210 microM) and a higher Vmax. Adrenalectomy did not affect activity in homogenates from controls, but partially reversed the diabetes-associated increase. Glucagon pretreatment of controls did not affect activity. In summary, distinct mitochondrial and cytosolic enzymes decarboxylate alpha-ketoisocaproate in liver. The increased hepatic capacity of diabetic rats to degrade the carbon skeleton of leucine is attributed mainly to a relative increase in mitochondrial mass.

Renal Hypertrophy in Streptozotocin-Diabetic Rats

1976 ◽  
Vol 51 (6) ◽  
pp. 551-555 ◽  
Author(s):  
K. Seyer-Hansen
Keyword(s):  
Weight Gain ◽  
Protein Content ◽  
Dna Content ◽  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Streptozotocin Diabetic Rats ◽  
Rna And Dna

1. Kidney weight and content of protein, RNA and DNA were measured in rats with streptozotocin diabetes of varying duration. 2. Diabetic rats had larger kidneys than control rats: after 3 days of diabetes the weight increase was 15% and after 42 days of diabetes it was 90%. The protein content rose in parallel to the weight. 3. RNA content was already increased after 36 h of glycosuria, whereas DNA content was unchanged for the first 3 days of diabetes, and increased thereafter. The protein/DNA ratio increased rapidly during the first 3 days but remained constant thereafter. 4. Insulin treatment decreased the renal weight gain by about 67% during the first 8 days of diabetes, but did not prevent the increase in DNA. When insulin was started after 25 days of diabetes there was only a slight regression of kidney growth.

Lipid peroxidation in early experimental diabetes in rats: effects of diabetes and insulin

1992 ◽  
Vol 126 (5) ◽  
pp. 378-380 ◽  
Author(s):  
Jørgen Rungby ◽  
Allan Flyvbjerg ◽  
Herdis B Andersen ◽  
Kirsten Nyborg
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Degradation Product ◽  
Insulin Treatment ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Early Stages

The degree of lipid peroxidation was measured in organs from diabetic rats receiving no treatment, and in those from insulin-treated diabetic rats and controls. Lipid peroxidation was measured as organ content of malondialdehyde, a degradation product of polyunsaturated fatty acids. In the kidney, lipid peroxidation was increased after one week of diabetes; insulin treatment reduced the level of lipid peroxidation to levels lower than seen in controls. In the liver, diabetes caused an increased lipid peroxidation, which could be reversed by insulin; no additional effect of insulin was found. In heart and pancreas no effects of diabetes or insulin were demonstrated. The present paper provides evidence that lipid peroxidation is increased in the early stages of experimental diabetes and is reversible by insulin treatment. Hyperinsulinaemia may, in itself, counteract lipid peroxidation in kidney.

Biomechanical and Microstructural Response of Recurrent Laryngeal Nerve in Pigs

2013 ◽  
Author(s):  
Megan Williams ◽  
Julie Barkmeier-Kraemer ◽  
Urs Utzinger ◽  
Jonathan Vande Geest
Keyword(s):  
Recurrent Laryngeal Nerve ◽  
Aortic Arch ◽  
Biomechanical Testing ◽  
Tensile Loading ◽  
Vocal Folds ◽  
Biomechanical Properties ◽  
Laryngeal Nerve ◽  
Nerve Tissue ◽  
Connective Tissues ◽  
Biomechanical Response

Tensile loading is a common physiological condition of peripheral nerves but can induce pathologic effects. Significant defects in nerve conduction have been reported for strains as low as ∼6% greater than the in situ strain [1]. In order to better understand the functional deficits resulting from tensile loading of nerve tissue, biomechanical testing is performed. The long-term goal of this research is to develop a constitutive and a computational model of the biomechanical properties of the “packaging,” or connective tissues of the recurrent laryngeal nerve (RLN) to investigate their role in the onset of unilateral vocal fold paralysis (UVP). The vocal folds are important for protection of the airway during swallowing, the regulation of breathing, and for voice production. Although surgery is most often linked to onset of UVP, the cause remains unknown in a large percentage of those with this disorder. Recent research has suggested that individuals with idiopathic UVP may have damage to the RLN at the level of the aortic arch related to a thoracic aneurysm. Our preliminary work has resulted in the conclusion that connective tissues of the RLN exhibit different biomechanical properties in the region of the aortic arch [2]. An aneurysm would impose increased stress and strain on the RLN where it is adjacent to the aorta resulting in impaired nerve function. The primary goal of this study is to identify the relationship between the biomechanical response of RLN tissue and how it response is governed by load dependent underlying extracellular matrix (collagen) organization. We hypothesize that regional differences exist in the microstructure and/or biomechanical response of the RLN and that these differences play a role in the onset of idiopathic UVP.

Inhibition of renal ornithine decarboxylase activity prevents kidney hypertrophy in experimental diabetes

1993 ◽  
Vol 264 (2) ◽  
pp. C453-C456 ◽  
Author(s):  
S. B. Pedersen ◽  
A. Flyvbjerg ◽  
B. Richelsen
Keyword(s):  
Ornithine Decarboxylase ◽  
Insulin Treatment ◽  
Experimental Diabetes ◽  
Selective Inhibition ◽  
Diabetic Rats ◽  
Decarboxylase Activity ◽  
Kidney Weight ◽  
Renal Enlargement ◽  
Diabetes Induction

The selective ornithine decarboxylase (ODC) inhibitor difluoromethyl ornithine (DFMO) was used to investigate the role of polyamines in initial diabetic renal enlargement. ODC activity in kidneys from diabetic animals was increased (fivefold) 24 h after diabetes induction (P < 0.05), and throughout the study (7 days) the activity remained 2- to 3-fold elevated (P < 0.05). Insulin treatment normalized renal ODC activity, whereas DFMO treatment totally inhibited the kidney ODC activity. The kidney weight in diabetic rats was 21% higher than that of control rats (1,074 +/- 35 mg and 889 +/- 16 mg, P < 0.001). Insulin treatment normalized kidney weight (847 +/- 13 mg). Despite unaltered diabetic metabolic aberrations the kidney weight in DFMO-treated diabetic rats was normalized (911 +/- 7 mg). In conclusion, the ODC activity in diabetic kidneys undergoing hypertrophy was increased. Insulin treatment normalized both kidney weight and kidney ODC activity. Finally, selective inhibition of ODC activity by DFMO resulted in kidneys of normal size, despite unaltered diabetic metabolic aberrations. These findings support the hypothesis that polyamines play an important role in initial diabetic renal enlargement.

Influence of experimental diabetes and insulin treatment on the enantioselective pharmacokinetics of mexiletine and its metabolites

2014 ◽  
Vol 92 (3) ◽  
pp. 263-266
Author(s):  
Ana Leonor Pardo Campos Godoy ◽  
Edson Z. Martinez ◽  
Maria Paula Marques ◽  
Andréia de Carvalho Leone ◽  
Eduardo Barbosa Coelho ◽  
...  
Keyword(s):  
Body Mass ◽  
Insulin Treatment ◽  
Experimental Diabetes ◽  
Area Under The Curve ◽  
Diabetic Rats ◽  
Control Group ◽  
Blood Collection ◽  
Glucose Levels ◽  
Streptozotocin Induced Diabetes ◽  
Enantioselective Pharmacokinetics

This study evaluates the influence of streptozotocin-induced diabetes on the kinetic disposition and metabolism of mexiletine (MEX) enantiomers in rats. Animals in the control (n = 6 for each blood collection time), diabetic (single intravenous dosage of 45 mg·(kg body mass)−1 of streptozotocin), and insulin-treated groups (diabetic rats treated daily with 2 IU insulin) received by gavage a single dose of 10 mg·(kg body mass)−1 racemic MEX. MEX enantiomers and the metabolites hydroxymethylmexiletine (HMM) and p-hydroxymexiletine PHM) were analyzed by LC-MS/MS. Statistical analysis was based on a serial sacrifice design, and parameter estimation was performed using a Bayesian modeling procedure. Area under the curve (AUC) for the (−)-(R) enantiomers of MEX, HMM, and PHM did not differ between the control and diabetic groups. However, AUC for (+)-(S)-MEX and (+)-(S)-HMM were lower in the diabetic than in the control group. Insulin treatment recovered glucose levels to normal and the (+)-(S)-MEX AUC and (+)-(S)-HMM AUC became similar to the AUCs observed in the nondiabetic animals.

Early changes in thyroid hormone metabolism in the heart, liver, and brown adipose tissue during the induction of low T3 syndrome in streptozotocin-diabetic rats

1990 ◽  
Vol 123 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Liv S. Bjørn-Hansen Gøtzsche ◽  
Ole Gøtzsche ◽  
Allan Flyvbjerg ◽  
Niels Boye
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Insulin Treatment ◽  
In Vitro Study ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Deiodinase Activity ◽  
Low T3 ◽  
Brown Adipose

Abstract. In order to elucidate the day-by-day development of low T3 syndrome, we made rats diabetic by an injection of streptozotocin. Untreated controls killed at day 0 and rats treated for 8 days with insulin after they had received streptozotocin served as controls. Subgroups of animals were killed 1, 2, 3, 4 and 8 days after streptozotocin. In serum, heart and liver, T3 was depressed to less than 50% of controls at day 4, whereas the insulin-treated rats differed from controls only as to heart T3. Heart iodothyronine 5'-deiodinase activity was depressed to a minimum at day 3 and depression was not prevented by insulin. Liver iodothyronine 5'-deiodinase activity had not reached a minimum at day 8, and again, insulin treatment did not normalize this parameter. T3 contents and iodothyronine 5'-deiodinase activity in brown adipose tissue did not differ from values in controls at any point of time. Thus, in the rats with low T3 syndrome induced by streptozotocin-diabetes, a lowered iodothyronine 5'-deiodinase activity is not fully inhibited by insulin treatment, whereas the T3 content in the liver is re-established during an observation period of 8 days. A direct toxic effect of streptozotocin seems unlikely as an in vitro study showed no influenze of streptozotocin on iodothyronine 5'-deiodinase activity in the liver. The study thus indicates that iodothyronine 5'-deiodinase activity in the heart and liver is depressed in experimental diabetes, despite near optimal regulation of blood glucose, and we suggest that lowered intracellular T3 production could, after some time, result in a hypothyroid state in different tissues.

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