STIMULATION BY STEROIDS AND AGE-DEPENDENT CHANGES OF L-CYSTINE ARYLAMIDASE ACTIVITY IN THE HYPOTHALAMUS OF THE RAT

1974 ◽  
Vol 76 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Herbert Kuhl ◽  
Christian Rosniatowski ◽  
Martin Bickel ◽  
Hans-Dieter Taubert

ABSTRACT L-cystine arylamidase activity was found to be high in hypothalamic homogenates from 10 day old rats, and then to decrease significantly until sexual maturity was reached (P < 0.01). This enzyme activity could be stimulated by treating 10 to 35 day old male rats with 100 μg of testosterone. Contrary to this, L-cystine arylamidase activity could not be stimulated in female animals by the injection of 7 μg of ethinyl-oestradiol before Day 45 of life. These data are interpreted as meaning that the L-cystine arylamidase activity plays a rôle in the processes regulating sexual maturation.

Author(s):  
Marziyeh Feyzi ◽  
Mohammad Reza Tabandeh ◽  
Mehrdad Shariati ◽  
Mohammad Amin Edalatmanesh

Introduction: Adiponectin is one of the most important adipose derived hormone that conflicting data are available about serum changes of adiponectin at different ages.The present study was done to determine the age related changes in serum adiponectin and its association with insulin resistance (IR) indices in aging in male rats. Methods: In this study, serum samples were obtained from male rats at different ages, including 2, 5, 10, 18, 52 and 72 weeks age (n=10 in each age group). Oral glucose tolerance and glucose stimulated insulin secretion tests were measured using determination of glucose concentrations at 15, 30, 45 and 60 min after oral ingestion of glucose (1 mg/kg body weight) for each animal. Serum adiponectin and insulin levels were determined using species specific ELISA kits. HOMA-IR was calculated based on glucose and insulin concentrations. Data were analyzed using SPSS version 16 software (SPSS Inc., Chicago, IL) also using one way analysis of variance and LSD posthoc tests. Results: Our results showed an age dependent decrease in serum adiponectin concentration, and 72-week old rats had the lowest level of adiponectin compared with those in other ages (p<0.05). IR indices, including fasting glucose, insulin, HOMA-IR and response to oral glucose ingestion was increased in an age dependent manner and 72-week old rats showed the highest levels of the IR indices. Conclusion: Regarding the role of adiponectin in glucose homeostasis and insulin sensitization, it seems that reduction of serum adiponectin with age progression may be an important mechanism of insulin resistance in aging.


1977 ◽  
Vol 86 (1) ◽  
pp. 60-70 ◽  
Author(s):  
Herbert Kuhl ◽  
Christian Rosniatowski ◽  
Hans-Dieter Taubert

ABSTRACT It had previously been shown that a luteinizing hormone-releasing hormone (LH-RH)-inactivating enzyme in the rat hypothalamus, L-cystine arylamidase, is in all probability involved in the short-loop feedback mechanism of LH. Since this enzyme system was also shown to be present in the pituitary, the effect of the iv injection of several sex hormones upon its activity was investigated. The basal arylamidase activity was found to be considerably higher in the neurohypophysis as compared to the adenohypophysis. The injection of 10 μg LH brought about a significant rise in arylamidase activity (+60 %) only in the latter. There was a dose-dependent increase in the pituitary enzyme activity 2 h after the iv administration of LH, and 16 h after the injection of oestradiol and progesterone into dioestrous rats. Contrary to previous findings obtained with hypothalamic homogenates, the effect of LH upon the enzyme in the pituitary proved to be not dependent on the presence of sex steroids, as the iv application of 10 μg LH into ovariectomized rats resulted in an increase of pituitary L-cystine arylamidase by about 30 %. The injection of testosterone, oestradiol and - to a lesser degree - progesterone into adult male rats caused a significant increase of enzyme activity in the hypophysis. Progesterone proved to be ineffective in the hypothalamus. This indicates that in contrast to the hypothalamus there is no sex-specific response of the LH-RH-degrading enzyme in the pituitary. It is concluded that this enzyme system seems to play an important part in the mechanisms regulating gonadotrophin release in the pituitary.


1987 ◽  
Vol 253 (3) ◽  
pp. E277-E282 ◽  
Author(s):  
S. M. Graham ◽  
P. A. Herring ◽  
I. J. Arinze

The effect of age on catecholamine regulation of hepatic glycogenolysis and on hepatic adenylate cyclase was studied in male rats up to 24 mo of age. Epinephrine and norepinephrine stimulated glycogenolysis in isolated hepatocytes at all age groups studied. Isoproterenol, however, stimulated glycogenolysis only at 24 mo. In isolated liver membranes, usual activators of adenylate cyclase increased the activity of the enzyme considerably more in membranes from 24-mo-old rats than in membranes from either 3- or 21-mo-old rats. The Mn2+-dependent activity of the cyclase was increased by 2.9-fold in 3-mo-old animals and approximately 5.7-fold in 24-mo-old rats, indicating a substantial age-dependent increase in the intrinsic activity of the catalytic unit. The density of the beta-adrenergic receptor, as measured by the binding of [125I]-iodocyanopindolol to plasma membranes, was 5-8 fmol/mg protein in rats aged 3-12 mo but increased to 19 fmol/mg protein in 24-mo-old rats. Computer-aided analysis of isoproterenol competition of the binding indicated a small age-dependent increase (from 30% at 3 mo to 43% at 24 mo) in the proportion of beta-receptors in the high-affinity state. These observations suggest that beta-receptor-mediated hepatic glycogenolysis in the aged rat is predicated upon increases in the density of beta-receptors as well as increased intrinsic activity of the catalytic unit of adenylate cyclase.


2000 ◽  
Vol 41 (6) ◽  
pp. 985-990 ◽  
Author(s):  
Birthe Moesgaard ◽  
Gitte Petersen ◽  
Jerzy W. Jaroszewski ◽  
Harald S. Hansen

1990 ◽  
Vol 126 (3) ◽  
pp. 461-466 ◽  
Author(s):  
M. N. Sillence ◽  
R. G. Rodway

ABSTRACT The effects of trenbolone acetate (TBA) on growth and on plasma concentrations of corticosterone were examined in male and female rats. At 5 weeks of age, rats were injected with TBA (0·8 mg/kg) dissolved in peanut oil, or with oil alone, daily for 10 days. In female rats, TBA caused an increase in weight gain (20–38%), a reduction in adrenal weight (19%) and a reduction in plasma concentrations of corticosterone (55%). In contrast, TBA-treated male rats showed no significant increase in weight gain, no significant change in adrenal weight and no reduction in plasma concentrations of corticosterone. The mechanism by which adrenal activity was suppressed in TBA-treated female rats was examined and the response compared with that to testosterone. Female rats (8 weeks old) were injected daily either with oil vehicle, TBA (0·8 mg/kg) or testosterone propionate (0·8 mg/kg). Testosterone increased weight gain (24%), but the growth response to TBA treatment was significantly greater (97%). A reduction in plasma concentrations of corticosterone (45%) was again observed in response to TBA. However, testosterone increased plasma concentrations of corticosterone (52%) above those of control values. Neither androgen affected plasma concentrations of ACTH. Finally, the effects of TBA were examined in 6-week-old female rats, to characterize further the apparent age-related increase in responsiveness. The growth response of 6-week-old rats (60–74%) was intermediate between that seen in 5- and 8-week-old animals. It is concluded that part of the anabolic activity of TBA may be related to a reduction in circulating concentrations of corticosterone. The effect of TBA on corticosterone concentrations differs from that of the natural androgen, testosterone, and does not appear to be mediated by a reduction in plasma concentrations of ACTH. Journal of Endocrinology (1990) 126, 461–466


1971 ◽  
Vol 66 (2) ◽  
pp. 221-228 ◽  
Author(s):  
Dona A. Frith ◽  
K. C. Hooper

ABSTRACT The previous paper (Frith & Hooper 1971) described the activities of certain hypothalamic enzymes at various times after mating and it was suggested that changes in enzymes levels may be used as an index of the release of gonadotrophic hormones. Using this approach, a study has been made of the action of the ovulation inhibitors chlormadinone acetate, norethindrone, ethinyl oestradiol and oestrone on the rabbit hypothalamus. The four inhibitors increased enzyme activity in the hypothalamus. Previous work has shown that raised levels of enzyme activity are associated with a lowered level of gonadotrophic hormone secretion. It is suggested, therefore, that one of the sites of action of the inhibitors is on polypeptide turnover in the hypothalamus, and it seems possible that this is one of the factors controlling the availability of gonadotrophin releasing factors.


1995 ◽  
Vol 269 (6) ◽  
pp. E983-E990 ◽  
Author(s):  
R. Perfetti ◽  
C. M. Rafizadeh ◽  
A. S. Liotta ◽  
J. M. Egan

Aging is an etiologic factor in non-insulin-dependent diabetes mellitus. To characterize the beta-cell abnormalities that occur with age, we investigated glucose-stimulated insulin release, pancreatic insulin content, and mRNA levels for islet-specific genes in aging Wistar rats. Ten minutes after glucose stimulation, 6-mo-old islets had approximately 40% more cells secreting insulin than 24-mo-old islets (P < 0.0001); after 1 h, 67 +/- 1.0% islets from 6-mo-old rats secreted insulin, compared with 51 +/- 3.5% from 24-mo-old rats (P < 0.0001). The amount of insulin secreted by each beta-cell was also less in the older animals (P < 0.0001). Despite increases in islet size (P < 0.0001) and beta-cell number (P < 0.0001) with age, whole pancreas insulin content showed that 24-mo-old pancreas had less insulin than 6-mo-old pancreas (0.61 +/- 0.06 vs. 0.84 +/- 0.08 microgram/mg pancreatic protein; P < 0.05). Finally, insulin mRNA levels declined to 50% of the newborn value in 24-mo-old islets (P < 0.0001), whereas glucagon mRNA levels showed a very modest decline with age. Somatostatin mRNA levels did not vary significantly. In summary, it appears that in Wistar rats there is a progressive decline in beta-cell activity with age. This decline may represent the biological features of the age-dependent risk of developing diabetes.


1998 ◽  
Vol 84 (2) ◽  
pp. 593-598 ◽  
Author(s):  
Michael K. Connor ◽  
David A. Hood

Connor, Michael K., and David A. Hood. Effect of microgravity on the expression of mitochondrial enzymes in rat cardiac and skeletal muscles. J. Appl. Physiol. 84(2): 593–598, 1998.—The purpose of this study was to examine the expression of nuclear and mitochondrial genes in cardiac and skeletal muscle (triceps brachii) in response to short-duration microgravity exposure. Six adult male rats were exposed to microgravity for 6 days and were compared with six ground-based control animals. We observed a significant 32% increase in heart malate dehydrogenase (MDH) enzyme activity, which was accompanied by a 62% elevation in heart MDH mRNA levels after microgravity exposure. Despite modest elevations in the mRNAs encoding subunits III, IV, and VIc as well as a 2.2-fold higher subunit IV protein content after exposure to microgravity, heart cytochrome c oxidase (CytOx) enzyme activity remained unchanged. In skeletal muscle, MDH expression was unaffected by microgravity, but CytOx activity was significantly reduced 41% by microgravity, whereas subunit III, IV, and VIc mRNA levels and subunit IV protein levels were unaltered. Thus tissue-specific (i.e., heart vs. skeletal muscle) differences exist in the regulation of nuclear-encoded mitochondrial proteins in response to microgravity. In addition, the expression of nuclear-encoded proteins such as CytOx subunit IV and expression of MDH are differentially regulated within a tissue. Our data also illustrate that the heart undergoes previously unidentified mitochondrial adaptations in response to short-term microgravity conditions more dramatic than those evident in skeletal muscle. Further studies evaluating the functional consequences of these adaptations in the heart, as well as those designed to measure protein turnover, are warranted in response to microgravity.


2009 ◽  
Vol 203 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Lidong Zhai ◽  
Joseph L Messina

Injuries, hemorrhage, sepsis, burn, and critical illnesses all induce insulin resistance, and insulin resistance is strongly associated with advancing age. However, the effect of age on injury induced insulin resistance is not well studied. We performed surgical trauma in male rats of three different ages (3-, 6-, and 10-weeks old). Rats were either hemorrhaged to a mean arterial pressure of 35–40 mmHg and subsequently maintained at that pressure for up to 90 min, or maintained without hemorrhage as controls. Results indicate that insulin-induced intracellular signaling was diminished in liver and skeletal muscle of 6- and 10-week old rats following trauma and hemorrhage. In even younger rats, immediately post-weaning (∼3 weeks of age), insulin signaling was lost in liver, but not in skeletal muscle. Glucocorticoids can play a role in the chronic development of insulin resistance. Our results demonstrate that corticosterone levels were increased in 6- and 10-week old animals following hemorrhage, but little change was measured in 3-week old animals. Blockade of glucocorticoid synthesis prevented the development of insulin resistance in skeletal muscle, but not in liver of 6- and 10-week old rats. Moreover, skeletal muscle glucocorticoid receptor levels increased dramatically between 3 and 6 weeks of age. These results indicate that trauma and hemorrhage-induced hepatic insulin resistance occurs at all ages tested. However, there is no development of insulin resistance following trauma and hemorrhage in skeletal muscle of post-weaning rats. In skeletal muscle of 6- and 10-week old rats, inhibition of glucocorticoid levels prevents the development of insulin resistance.


1979 ◽  
Vol 180 (2) ◽  
pp. 313-318 ◽  
Author(s):  
Coral A. Lamartiniere ◽  
Cindy S. Dieringer ◽  
Etsuko Kita ◽  
George W. Lucier

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.


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