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.

Blood flow elevation increases VO2 maximum during repetitive tetanic contractions of dog muscle in situ

1993 ◽  
Vol 74 (4) ◽  
pp. 1499-1503 ◽  
Author(s):  
W. F. Brechue ◽  
B. T. Ameredes ◽  
G. M. Andrew ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Power Production ◽  
Arterial Supply ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Control Series ◽  
Flow Through ◽  
Series Of Experiments

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.

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 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.

Increased sciatic nerve blood flow in diabetic rats: assessment by "molecular" vs. particulate microspheres

1997 ◽  
Vol 273 (1) ◽  
pp. E164-E173 ◽  
Author(s):  
K. Chang ◽  
Y. Ido ◽  
W. LeJeune ◽  
J. R. Williamson ◽  
R. G. Tilton
Keyword(s):  
Blood Flow ◽  
Sciatic Nerve ◽  
Reference Sample ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Nerve Blood Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Microsphere Method ◽  
Onset Of Diabetes

Sciatic nerve blood flow in diabetic rats in typically increased or unchanged when assessed by the reference sample microsphere method in our laboratory. In contrast, blood flow is generally reported to be decreased approximately 50% when assessed with laser Doppler flowmetry or hydrogen clearance polarography. To address concerns that increased blood flow observed with microspheres might be anomalous because of their particulate nature and/or because insufficient numbers of microspheres are captured in the nerve, a plasma-soluble "molecular microsphere" ([3H]desmethylimipramine, mol wt = 266) and 11.3-micron 153Gd-labeled microspheres were injected sequentially to assess blood flow in rats with streptozotocin diabetes of 2-4 wk duration. Nerve blood flows in diabetic rats were increased 1.5- to 2-fold (vs. control rats) with both tracers; these increases were prevented by tolrestat, an inhibitor of aldose reductase. These observations indicate that blood flow in sciatic nerve (like that in retina and kidney) is increased early after the onset of diabetes and is 1) demonstrable with a plasma-soluble tracer as well as with particulate microspheres and 2) linked to increased metabolism of glucose via the sorbitol pathway.

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.

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.

scholarly journals Reproductive Disorders in Streptozotocin-Treated Male Rats Following Co-Administration of Ethambutol, Rifampicin, Isoniazid and Pyrazinamide

2012 ◽  
Vol 19 (4) ◽  
pp. 405-415
Author(s):  
Ganna M. Shayakhmetova ◽  
Larysa B. Bondarenko ◽  
Anatoliy V. Matvienko ◽  
Valentina M. Kovalenko
Keyword(s):  
Dna Fragmentation ◽  
Streptozotocin Diabetes ◽  
Reproductive Organs ◽  
Diabetic Rats ◽  
Male Rats ◽  
Male Rat ◽  
Offspring Survival ◽  
Reproductive Disorders ◽  
Offspring Development ◽  
Qualitative Changes

AbstractObjectives: To evaluate the effect of anti-tuberculosis drugs (ATD) on indices ofreproductive capability, DNA fragmentation and offspring development of male ratswith testicular malfunction caused by experimental diabetes. Materials and Methods: Wistar albino male rats (body weight 160-200 g) were divided into threegroups: I - control, II - streptozotocin diabetes, III - streptozotocin diabetes + ATD.The testis DNA fragmentation was determined electrophoretically; spermatogeneticindices, offspring antenatal and postnatal development indices - by standardprocedures. Morphological analyses of gonadic structures were carried out by opticmicroscopy. Results: The study of the effects of diabetes and ATD administration ontestis cells morphologic and morphometric parameters and spermatogenesissuggested the presence of specific diabetes- and anti tuberculosis drugs - mediatedquantitative and qualitative changes in male rat reproductive organs,spermatogenetic epithelial cells, level and character of DNA fragmentation incomparison with normal rats. These changes were accompanied by alterations inprocesses of fertilisation (with intact females), embryogenesis and by lowering ofoffspring survival. Conclusions: Observed changes could hence affect the state andcorrect functioning of spermatogenetic epithelium and of other tissues ofreproductive organs, as well as offspring development in diabetic rats.

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.

Progressive and concurrent deterioration of vagus-stimulated and hypoglycemia-induced glucagon secretion in streptozotocin-diabetic rats

1992 ◽  
Vol 126 (1) ◽  
pp. 80-84 ◽  
Author(s):  
Zsolt I Hertelendy ◽  
DG Patel ◽  
Kenneth A Skau
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Parasympathetic Nervous System ◽  
Matched Control ◽  
Streptozotocin Diabetes ◽  
Glucagon Secretion ◽  
Diabetic Rats ◽  
Male Rats ◽  
Streptozotocin Diabetic Rats

The effects of left cervical vagus nerve stimulation on glucagon secretion were studied in streptozotocin-diabetic and age-matched control adult male rats. At two-week intervals, after the induction of streptozotocin-diabetes, streptozotocin-diabetic and age-matched control rats were anesthetized with chloral hydrate (350 mg/kg, ip). Left cervical vagus nerves were electrically stimulated via a Grass stimulator with 5-volt monophasic pulses of 3 msec duration at a frequency of 20 Hz for 1, 2, and 4 min. Arginine-induced glucagon secretion was also determined. Vagus nerve-stimulated (2 and 4 min) glucagon secretion deteriorated as the duration of streptozotocin-diabetes increased. Glucagon secretion in response to vagus nerve stimulation was virtually absent by 12 weeks of streptozotocin-diabetes. However, arginine-induced glucagon secretion was unaffected. Subsequent experiments showed that the defect in glucagon secretion from vagal stimulation occurred concurrently with that seen from insulin-induced hypoglycemia. These results indicate that the impaired hypoglycemia-induced glucagon secretion in long-term streptozotocin-diabetic rats may be correlated with the deterioration of the parasympathetic nervous system transmission in streptozotocin-diabetes.

Growth hormone-releasing factor expression is discordantly regulated in the hypothalamus and testis of streptozotocin-diabetic rats

1996 ◽  
Vol 148 (2) ◽  
pp. 189-192 ◽  
Author(s):  
D Olchovsky ◽  
J F Bruno ◽  
M Berelowitz
Keyword(s):  
Growth Hormone ◽  
Mrna Expression ◽  
Arcuate Nucleus ◽  
Insulin Treatment ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Diabetic Rats ◽  
Male Rats ◽  
Mrna Levels ◽  
Growth Hormone Releasing Factor

Abstract Growth hormone-releasing factor (GRF) mRNA expression in male rats occurs predominantly in the hypothalamus (mainly in the arcuate nucleus), and among extraneural sites primarily in the testis. Hypothalamic GRF is the physiological tropic stimulus to growth hormone secretion. However, the role of GRF in the testis is unknown. We have shown previously that hypothalamic GRF mRNA expression is significantly reduced in streptozotocin (STZ)-diabetic rats. This reduction is confined to the arcuate nucleus and probably accounts for the suppression of growth hormone pulsatility. The present studies were performed to evaluate GRF expression in the testis of streptozotocin (STZ)-diabetic rats. Diabetes was induced by injection of STZ (100 mg/kg i.p.). Seventeen to twenty days later diabetic rats were hyperglycemic compared with vehicle-injected controls and demonstrated growth failure. Insulin treatment reduced the glycemia and increased body weight towards normal. Total RNA was extracted from the hypothalamus and testis, and GRF mRNA levels estimated by solution hybridization/nuclease protection assay. Levels of hypothalamic somatostatin mRNA were measured to serve as control values. GRF mRNA was significantly (P<0·001) decreased in the hypothalamus of STZ-diabetic rats (0·2 ± 0·07 mean relative densitometric units, n=8) compared with controls (1·0 ± 0·19, n=8) with no change in somatostatin mRNA expression. In contrast, testicular GRF mRNA was increased 70% (P<0·05) in STZ-diabetic rats. Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1·1 ± 0·17, n=5) with no effect on testicular GRF mRNA expression. In conclusion GRF gene expression is discordantly regulated in tissues of male STZ-diabetic rats. While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. Journal of Endocrinology (1996) 148, 189–192

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