scholarly journals Age-Related Alteration in Serum Adiponectin in Rats and Its Association with Insulin Resistance Markers

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.

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


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
James Moore ◽  
Rashid Akbergenov ◽  
Martina Nigri ◽  
Patricia Isnard-Petit ◽  
Amandine Grimm ◽  
...  

AbstractRandom errors in protein synthesis are prevalent and ubiquitous, yet their effect on organismal health has remained enigmatic for over five decades. Here, we studied whether mice carrying the ribosomal ambiguity (ram) mutation Rps2-A226Y, recently shown to increase the inborn error rate of mammalian translation, if at all viable, present any specific, possibly aging-related, phenotype. We introduced Rps2-A226Y using a Cre/loxP strategy. Resulting transgenic mice were mosaic and showed a muscle-related phenotype with reduced grip strength. Analysis of gene expression in skeletal muscle using RNA-Seq revealed transcriptomic changes occurring in an age-dependent manner, involving an interplay of PGC1α, FOXO3, mTOR, and glucocorticoids as key signaling pathways, and finally resulting in activation of a muscle atrophy program. Our results highlight the relevance of translation accuracy, and show how disturbances thereof may contribute to age-related pathologies.


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.


1995 ◽  
Vol 268 (4) ◽  
pp. C952-C957 ◽  
Author(s):  
J. Yannariello-Brown ◽  
S. H. Chapman ◽  
W. F. Ward ◽  
T. C. Pappas ◽  
P. H. Weigel

Circulating hyaluronan (HA) levels were investigated as a function of age and diet in Fischer 344 male rats. A biphasic pattern of age-related changes was observed in rats fed ad libitum a diet in which the protein source was soya/fish meal. HA levels in 3- to 6- and 22- to 29-mo-old rats were not statistically different. However, HA levels in 12- to 20-mo-old rats were 10-29% of the levels in younger or aged adults. HA levels were also measured in rats fed ad libitum a semisynthetic diet in which the protein source was hydrolyzed casein. Whereas the two colonies exhibited similar biphasic age-related changes, HA levels differed 4- to 20-fold at every age examined. Caloric restriction affected HA levels in 19-mo-old casein-fed rats; HA levels were 2.3 times higher than age-matched controls and were not statistically different from young or aged animals. Serum and plasma HA levels were identical in the same individuals at all ages tested. These data suggest that HA turnover and metabolism in the rat are affected by age, dietary composition, and caloric intake.


1998 ◽  
Vol 85 (5) ◽  
pp. 1903-1908 ◽  
Author(s):  
Ronald R. Gomes ◽  
Frank W. Booth

We examined the age-related association in skeletal muscle between atrophy and expression of mRNAs encoding both the γ-subunit of the nicotinic acetylcholine receptor (AChR), and myogenin, a transcription factor that upregulates expression of the γ-subunit promoter. Gastrocnemius and biceps brachii muscles were collected from young (2-mo-old), adult (18-mo-old), and old (31-mo-old) Fischer 344/Brown Norway F1 generation cross male rats. In the gastrocnemius muscles of old vs. young and adult rats, lower muscle mass was accompanied by significantly elevated AChR γ-subunit and myogenin mRNA levels. In contrast, the biceps brachii muscle exhibited neither atrophy nor as drastic a change in AChR γ-subunit and myogenin mRNA levels with age. Expression of the AChR ε-subunit mRNA did not change with age in either gastrocnemius or biceps brachii muscles. Thus changes in skeletal muscle AChR γ-subunit and myogenin mRNA levels may be more related to atrophy than to chronological age in old rats.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Ayaka Domon ◽  
Kentaro Katayama ◽  
Yuki Tochigi ◽  
Hiroetsu Suzuki

A variety of animal models of diabetes mellitus (DM) are required to study the genetics and pathophysiology of DM. We established a novel rat strain showing nonobese type 2 diabetes with enlarged kidneys from the LEA.PET-pet congenic strain and named it Diabetes with Enlarged Kidney (DEK). The body growth of DEK affected rats was similar to that of normal rats before the development of DM but was attenuated with the deterioration of DM. There was a marked difference in the etiology of DEK by gender: DM phenotypes including polyuria, polydipsia, and hyperglycemia (nonfasting blood glucose over 300 mg/dl) were found in male rats aged over 10 weeks but not in female rats. The cumulative incidence of DM in DEK males at the age of 30 weeks was 44.8%. Oral glucose tolerance tests showed glucose intolerance and decreased insulin secretion in response to glucose loading in affected males, features which were exacerbated with age. Affected males exhibited disorganized architecture of pancreatic islets, decreased numbers of β cells, and markedly decreased expression of insulin, despite no pathological findings of hemorrhage or infiltration of inflammatory cells in the pancreatic islet. Age-related islet fibrosis appeared similar in normal and affected males. Affected males also showed enlarged kidneys with dilation of renal tubules in both the cortex and medulla, but no obvious glomerular lesions typical of diabetic nephropathy (DN) at the age of 30 weeks. Plasma levels of urea nitrogen and creatinine were normal, but hypoalbuminemia was detected. These pathophysiological features in affected males indicated that their renal function was almost maintained despite severe DM. Taken together, these findings indicate that the affected males of the DEK strain are a novel nonobese type 2 diabetes rat model useful for studying the mechanisms underlying β cell loss and identifying genetic factors protective against DN.


1987 ◽  
Vol 253 (1) ◽  
pp. G86-G92 ◽  
Author(s):  
Z. Gregus ◽  
A. F. Stein ◽  
C. D. Klaassen

The role of gamma-glutamyltransferase (GGT) in the biliary excretion of glutathione (GS) was studied in rats during postnatal development. Between 2 and 10 wk of age the biliary excretion of GS-related sulfur increased ninefold. During this period, alterations were observed in both hepatic GGT and the composition of GS-related thiols and disulfides in bile. For instance, between 3 and 4 wk of age, GGT activity and the biliary excretion of GS hydrolysis products (Cys-Gly and Cys) increased markedly, and the latter became the predominant sulfhydryls in bile. However, by 10 wk of age, the excretion rate of GS increased and exceeded the rate of excretion of Cys-Gly and Cys. The parallelism between hepatic GGT activity and the biliary excretion of GS-hydrolysis products during development suggests a role for GGT in the formation of biliary Cys-Gly and Cys. Furthermore, in 4-wk-old rats, inhibition of hepatic GGT by acivicin markedly decreased the biliary excretion of Cys-Gly and Cys and increased that of GS without influencing the excretion of total GS-related sulfur in bile. The biliary excretion of GS-related thiols was less responsive to acivicin in 2- and 7- to 10-wk-old rats, suggesting that GGT plays a smaller role in influencing biliary thiol composition at those ages. In summary, GS transported into bile is hydrolyzed in an age-dependent manner, however, the GGT-initiated hydrolysis of GS does not affect the biliary excretion of total thiols in rats.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Erika Vyskočilová ◽  
Barbora Szotáková ◽  
Lenka Skálová ◽  
Hana Bártíková ◽  
Jitka Hlaváčová ◽  
...  

Process of aging is accompanied by changes in the biotransformation of xenobiotics and impairment of normal cellular functions by free radicals. Therefore, this study was designed to determine age-related differences in the activities and/or expressions of selected drug-metabolizing and antioxidant enzymes in young and old rats. Specific activities of 8 drug-metabolizing enzymes and 4 antioxidant enzymes were assessed in hepatic subcellular fractions of 6-week-old and 21-month-old male Wistar rats. Protein expressions of carbonyl reductase 1 (CBR1) and glutathioneS-transferase (GST) were determined using immunoblotting. Remarkable age-related decrease in specific activities of CYP2B, CYP3A, and UDP-glucuronosyl transferase was observed, whereas no changes in activities of CYP1A2, flavine monooxygenase, aldo-keto reductase 1C, and antioxidant enzymes with advancing age were found. On the other hand, specific activity of CBR1 and GST was 2.4 folds and 5.6 folds higher in the senescent rats compared with the young ones, respectively. Interindividual variability in CBR1 activity increased significantly with rising age. We suppose that elevated activities of GST and CBR1 may protect senescent rats against xenobiotic as well as eobiotic electrophiles and reactive carbonyls, but they may alter metabolism of drugs, which are CBR1 and especially GSTs substrates.


2012 ◽  
Vol 37 (5) ◽  
pp. 997-1002
Author(s):  
Jose E. Galgani ◽  
Karla Vasquez ◽  
Giannella Leonelli ◽  
Alejandra Espinosa ◽  
Hector Araya ◽  
...  

The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Fifteen healthy, young (24 ± 5 years), nonobese (23 ± 2 kg·m–2), insulin-sensitive (ISI composite = 6.0 ± 1.2) individuals and 14 healthy, young (22 ± 2 years), nonobese (24 ± 2 kg·m–2), insulin-resistant (ISI composite = 2.7 ± 1.1) individuals received a 75 g oral glucose dose. Blood samples were drawn before and for 2 h after glucose ingestion for red blood cell glutathione and serum glucose and insulin concentrations. Glycemia before and after glucose ingestion was similar between groups (p = 0.17), which suggest that hyperinsulinemia compensated impaired insulin sensitivity. Red blood cell total (p = 0.81), reduced (p = 0.79), and oxidized (p = 0.88) glutathione concentrations were similar between groups under fasting and postprandial conditions. However, in response to glucose, increases in total and reduced glutathione concentrations were found at the end of the 2 h assessment period in both groups (p < 0.05). Direct associations between postprandial glucose response and red blood cell total (r = 0.52; p < 0.05) and oxidized (r = 0.61; p = 0.02) glutathione concentrations were observed only in insulin-sensitive subjects. In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions.


1984 ◽  
Vol 247 (5) ◽  
pp. R850-R855
Author(s):  
L. B. Poole ◽  
M. S. Liu ◽  
P. W. Landfield

Kinetic analyses of the Na+-K+-adenosine triphosphatase (ATPase) system were performed in brain and heart preparations from young mature (4 mo old) and healthy aged (25 mo old) rats. The K+-activated p-nitrophenylphosphatase (K+-pNPPase) method was used to assess activity of the enzyme system. Ouabain inhibition of K+-pNPPase activity was also examined. A significant age-related decrease in maximal velocity (Vmax) was found in cardiac K+-pNPPase activity, but no changes were seen in the K+ concentration for half-maximal velocity (K0.5). No age differences in Vmax or K0.5 were seen for brain. No differences in ouabain inhibition were found in either brain or heart. In a second experiment, the major component of the age-related decline in cardiac K+-pNPPase activity was found to occur between 5 and 14 mo of age, a period during which plasma thyroxine had previously been found to decline in the same animals. Since peripheral Na+-K+-ATPase activity is partly thyroid hormone dependent, the age-dependent decrease in cardiac enzyme activity appears to be secondary to neuroendocrine changes.


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