Effects of exercise on insulin distribution and action in testosterone-treated oophorectomized female rats

2000 ◽  
Vol 88 (6) ◽  
pp. 2116-2122 ◽  
Author(s):  
Maria Niklasson ◽  
Peter Daneryd ◽  
Peter Lönnroth ◽  
Agneta Holmäng
Keyword(s):  
Insulin Resistance ◽  
Physical Exercise ◽  
Insulin Action ◽  
Female Rats ◽  
Control Group ◽  
Free Access ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Severe Insulin Resistance ◽  
Ovx Rats ◽  
Running Wheels

Administration of testosterone (T) to oophorectomized (Ovx) female rats is followed by severe insulin resistance, localized to postreceptor cellular events in the muscle. In this study, intervention by exercise was introduced to examine whether circulatory adaptations are involved in insulin resistance. Two groups of Ovx rats were studied: one group was given T (Ovx+T); another group had free access to running wheels (Ovx+T+Ex). In addition, one control group (sham operated) was studied. Insulin sensitivity was measured with the euglycemic hyperinsulinemic clamp technique (submaximal) for 150 min. Muscle interstitial glucose and insulin concentrations were measured by microdialysis. The measurements showed that, in Ovx+T rats, the onset of insulin action was significantly ( P < 0.05) slower during the first 95 min of the clamp compared with that in Ovx+T+Ex and controls. Muscle interstitial concentrations of insulin but not glucose were lower in both Ovx+T and Ovx+T+Ex rats than in controls throughout the clamp. It was concluded that physical exercise prevented the slow onset of insulin action in Ovx+T rats without changing the distribution time of muscle interstitial insulin. The results indicate that hyperandrogenicity is characterized by delayed muscle insulin action. Physical exercise reverses these defects without any beneficial effect on muscle interstitial insulin concentrations.

Insulin action and resistance in obesity and noninsulin-dependent type II diabetes mellitus

1982 ◽  
Vol 243 (1) ◽  
pp. E15-E30 ◽  
Author(s):  
J. M. Olefsky ◽  
O. G. Kolterman ◽  
J. A. Scarlett
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Tissue Level ◽  
Dependent Diabetes Mellitus ◽  
Target Tissue ◽  
Severe Insulin Resistance ◽  
Glucose Clamp Technique

Resistance to the action of insulin can result from a variety of causes, including the formation of abnormal insulin or proinsulin molecules, the presence of circulating antagonists to insulin or the insulin receptor, or defects in insulin action at the target tissue level. Defects of the latter type are characteristic of obesity and of noninsulin-dependent diabetes mellitus. Analysis of the nature of the insulin resistance in those disorders has been investigated in intact subjects with the use of the euglycemic glucose clamp technique, and both insulin receptors and insulin-mediated glucose metabolism have been studied in adipocytes and monocytes from affected individuals. In both conditions, the cause of insulin resistance is heterogeneous. In some, insulin resistance appears to be due to a defect in the insulin receptor, whereas others have a defect both in the receptor and at the postreceptor level. In both groups, more severe insulin resistance is due to the postreceptor lesion and is correctable with appropriate therapy.

Insulin resistance caused by amylin in conscious rats is independent of induced hypocalcemia and fades during long-term exposure

1993 ◽  
Vol 129 (4) ◽  
pp. 360-365 ◽  
Author(s):  
Clemens Fürnsinn ◽  
Peter Nowotny ◽  
Michael Roden ◽  
Madeleine Rohac ◽  
Thomas Pieber ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Tolerance Test ◽  
Zucker Rats ◽  
Control Group ◽  
Short Term ◽  
Euglycemic Hyperinsulinemic Clamp

To compare the effect of short- vs long-term amylin infusion on insulin sensitivity, glucose tolerance and serum calcemia, euglycemic-hyperinsulinemic clamp (26 pmol·kg−1·min−1) and glucose tolerance tests (2.4 mmol/kg over 30 min) were performed in lean Zucker rats. Three infusion protocols were employed: control group: 24 h of iv saline; short-term amylin exposure: 22 h of iv saline followed by 2 h of iv amylin (20 μg/h); long-term amylin exposure: 24 h of iv amylin (20 μg/h). Insulin resistance was induced by short-term amylin infusion during euglycemic clamping, as shown by a 41% decrease in space-corrected glucose infusion rates (μmol·kg−1·min−1; control group, 106.0±15.0; short-term iv amylin, 62.7±15.0; p<0.00 5). After long-term amylin exposure, insulin sensitivity was identical to control values (109.9±6.7). This fading action of amylin was confirmed by data from the glucose tolerance test, demonstrating glucose intolerance after short- but not after long-term amylin exposure. Serum calcium concentration decreased during short-term (2 h) amylin infusion (from 2.52±0.15 to 2.09±0.12 mmol/l; p<0.01) and hypocalcemia of a similar extent also was present after 22 h and 24 h of amylin exposure (2.10±0.09 and 2.04±0.14 mmol/l, respectively). The data demonstrate that short-term amylin infusion induces insulin resistance and glucose intolerance, both of which vanish during long-term (>22 h) amylin exposure, being apparently independent of induced hypocalcemia.

scholarly journals Effects of Greenshell Mussel (Perna canaliculus) Intake on Pathological Markers of Multiple Phenotypes of Osteoarthritis in Rats

2020 ◽  
Vol 10 (17) ◽  
pp. 6131
Author(s):  
Parkpoom Siriarchavatana ◽  
Marlena C. Kruger ◽  
Matthew R. Miller ◽  
Hong (Sabrina) Tian ◽  
Frances M. Wolber
Keyword(s):  
Normal Control ◽  
Control Diet ◽  
Female Rats ◽  
Control Group ◽  
Sham Operation ◽  
High Fat ◽  
Mineral Density ◽  
Perna Canaliculus ◽  
High Sugar ◽  
Ovx Rats

The prevalence of metabolic osteoarthritis has been increasing worldwide, particularly among women. The aim of this study was to investigate the effects of the New Zealand greenshell mussel (Perna canaliculus; GSM) on osteoarthritis (OA) prevention in a rat model. One-hundred-and-eight female rats aged 12 weeks were divided into four test groups, containing 24 rats each, plus an additional control group. Each test group received one of the four experimental diets: normal control diet (ND), normal control diet supplemented with GSM (ND + GSM), high fat/high sugar diet (HFHS), or high fat/high sugar diet supplemented GSM (HFHS + GSM), for 36 weeks (end of the study). After 8 weeks on experimental diets, half of each group was subjected to ovariectomy (OVX) and the remaining half received a sham operation (ovaries left intact). The study evaluated body composition, bone mass, plasma cytokines, adipokines, HbA1c, CTX-II, and knee joint’s histopathology. HFHS diet and OVX significantly induced body weight gain and leptin production. OVX rats lost bone mineral density but increased adiponectin, HbA1C, and MCP-1. The OVX rats fed HFHS showed the highest Mankin scores. Importantly, inclusion of GSM reduced these pathological features. In conclusion, GSM might be beneficial in halting the progression of OA.

Sepsis-induced changes in in vivo insulin action in diabetic rats

1989 ◽  
Vol 257 (3) ◽  
pp. E301-E308 ◽  
Author(s):  
C. H. Lang ◽  
C. Dobrescu
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Plasma Concentrations ◽  
Diabetic Rats ◽  
Hepatic Insulin Resistance ◽  
Blood Levels ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Glucose Output

The present study examined whether sepsis exacerbates the diabetes-induced peripheral and hepatic insulin resistance. Vascular catheters were placed in diabetic (70 mg/kg streptozotocin, 4-wk duration) and nondiabetic rats, and sepsis was produced by subcutaneous injections of live Escherichia coli. Basal glucose metabolism was determined with the use of [3-3H]glucose initiated 18 h after the first injection of bacteria. Thereafter, in vivo insulin action was assessed with the use of the euglycemic hyperinsulinemic clamp technique. Sepsis in nondiabetic rats produced a 57% reduction in the maximal responsiveness for the insulin-induced increase in total glucose utilization compared with nondiabetic nonseptic animals. Diabetes alone decreased both insulin sensitivity and responsiveness. When the septic insult was superimposed on the diabetic condition, the maximum responsiveness was unchanged compared with non-septic diabetic rats, but the 50% maximally efficient dose was reduced from 817 to 190 microU/ml, suggesting an improvement in insulin sensitivity. Sepsis did not alter the insulin-induced suppression of hepatic glucose output in either nondiabetic or diabetic animals. Sepsis increased the plasma concentrations of epinephrine, norepinephrine, glucagon, and corticosterone in both nondiabetic and diabetic rats; however, the elevation in catecholamines and glucagon was 65 to 250% greater in the diabetic animals. These results indicate that hypermetabolic sepsis produces peripheral insulin resistance in nondiabetic rats but does not worsen the preexisting insulin resistance in diabetic animals, despite the higher prevailing blood levels of glucagon and catecholamines.

scholarly journals Effect of Testosterone Enanthate Modeling of Polycystic Ovary on Liver Irs-2 mRNA Expression in Rats: A Brief Report

2021 ◽  
Vol 18 (3) ◽  
pp. 0480
Author(s):  
Seyyed Amir Yasin Ahmadi ◽  
Mandana Beigi Boroujeni ◽  
Naser Pajouhi ◽  
Amin Hasanvand ◽  
Afshin Hasanvand ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Animal Models ◽  
Mrna Expression ◽  
Polycystic Ovary ◽  
Vehicle Group ◽  
Control Group ◽  
P Value ◽  
Free Access ◽  
Testosterone Enanthate ◽  
Significant Difference

There are many animal models for polycystic ovary (PCO); using exogenous testosterone enanthate is one of the methods of induction of these models. However, induction of insulin resistance should also be studied in the modeling technics. Therefore, the present study aims to investigate the expression of insulin receptor substrate (Irs)-2 mRNA in the liver tissue of rat PCO model. Nineteen Wistar rats were divided into three groups; (1) PCO modeling group (N =7) received daily 1.0 mg/100g testosterone enanthate solved in olive oil along with free access dextrose water 5%, (2) vehicle group (N =6), which handled like the PCO group, but did not receive testosterone enanthate, (3) control group (N =6) with standard care. All the animals were administered via intra-peritoneal injection for 14 days. Expression of Irs-2 mRNA was studied with real-time PCR and fold changes (FC) were reported. The average of expression in the control group was considered as the calibrator. About 13.4% expression reduction was found in the PCO group (FC =0.874, P-value =0.043). No significant reduction was found in the vehicle group (FC =0.951, P-value =0.076). However, analysis of variance did not show a significant difference between all the groups of study (P-value =0.085). The present model of PCO might induce insulin resistance at liver level with a low effect size via reduction in the mRNA expression of Irs-2. Study of the involved genes and molecules in other tissues of PCO animal models is suggested.

scholarly journals Evaluation of the Bone Morphology Around Four Types of Porous Metal Implants Placed in Distal Femur of Ovariectomized Rats

2020 ◽  
Author(s):  
Stanislav Bondarenko ◽  
Nataliya Ashukina ◽  
Valentyna Maltseva ◽  
Gennadiy Ivanov ◽  
Ahmed Amine Badnaoui ◽  
...  
Keyword(s):  
Bone Formation ◽  
Histological Study ◽  
Porous Metal ◽  
Structural Features ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Control Group ◽  
Implant Materials ◽  
Normal Bone ◽  
Ovx Rats

Abstract Background To compare structural features of femoral bone of ovariectomized and non-ovariectomized rats after implantation of porous materials (TANTALUM, CONCELOC, TTM, ATLANT). Methods Experiments were carried out on 56 white laboratory female rats aged 6-months. Rats were randomly assigned into groups: Sham control group (SH) or ovariectomy group (OVX). Four different commercial implant materials (TTM, CONCELOC, TANTALUM, ATLANT) were placed into the defects (diameter 2.5mm, depth 3.0mm) in the distal metaphysis of femurs. Rats were sacrificed 45-days after surgery. Histological study was performed and the percentage of bone area (BA%) around the implant at a distance of 500μm in the cancellous area was measured. Results Formation of mature bone tissue of varying degrees around all of the implants was detected. In OVX rats cancellous bone defect zone was characterized by a high density of osteocytes on the surface. In the SH group, no differences in BA% among implant materials were found. In OVX rats the BA% around ATLANT implants was 1.5-time less (p=0.002) than around TANTALUM. The BA% around the rest of the materials was not statistically different. Conclusions Bone formation around the studied porous titanium and tantalum materials in the osteoporosis model was lower than in normal bone. There were differences in bone formation around the different materials in the osteoporosis model, while in the normal bone model these differences were absent.

scholarly journals Continuous Administration of a P450 Aromatase Inhibitor Induces Polycystic Ovary Syndrome with a Metabolic and Endocrine Phenotype in Female Rats at Adult Age

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 434-445 ◽  
Author(s):  
Manuel Maliqueo ◽  
Miao Sun ◽  
Julia Johansson ◽  
Anna Benrick ◽  
Fernand Labrie ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Female Rats ◽  
Control Group ◽  
Ovary Syndrome ◽  
Continuous Administration ◽  
P450 Aromatase ◽  
Fat Depots ◽  
Estrogen Synthesis

Studying the mechanisms for the complex pathogenesis of polycystic ovary syndrome (PCOS) requires animal models with endocrine, reproductive, and metabolic features of the syndrome. Hyperandrogenism seems to be a central factor in PCOS, leading to anovulation and insulin resistance. In female rats, continuous administration of letrozole, a nonsteroidal inhibitor of P450 aromatase, at 400 μg/d starting before puberty induces hyperandrogenemia and reproductive abnormalities similar to those in women with PCOS. However, despite high circulating testosterone levels, these rats do not develop metabolic abnormalities, perhaps because of their supraphysiological testosterone concentrations or because estrogen synthesis is completely blocked in insulin-sensitive tissues. To test the hypothesis that continuous administration of lower doses of letrozole starting before puberty would result in both metabolic and reproductive phenotypes of PCOS, we performed a 12-wk dose-response study. At 21 d of age, 46 female Wistar rats were divided into two letrozole groups (100 or 200 μg/d) and a control group (placebo). Both letrozole doses resulted in increased body weight, inguinal fat accumulation, anovulation, larger ovaries with follicular atresia and multiples cysts, endogenous hyperandrogemia, and lower estrogen levels. Moreover, rats that received 200 μg/d had insulin resistance and enlarged adipocytes in inguinal and mesenteric fat depots, increased circulating levels of LH, decreased levels of FSH, and increased ovarian expression of Cyp17a1 mRNA. Thus, continuous administration of letrozole, 200 μg/d, to female rats for 90 d starting before puberty results in a PCOS model with reproductive and metabolic features of the syndrome.

scholarly journals Compensatory nutrition-directed mammary cell proliferation and lactation in rats

1998 ◽  
Vol 79 (2) ◽  
pp. 177-183 ◽  
Author(s):  
S. H. Kim ◽  
Y. S. Moon ◽  
W. L. Keller ◽  
C. S. Park
Keyword(s):  
Cell Proliferation ◽  
Growth Phase ◽  
Mammary Epithelial ◽  
Female Rats ◽  
Mammary Tissue ◽  
Control Group ◽  
Average Weight ◽  
Free Access ◽  
Lactation Performance ◽  
Mammary Cell

The proper use of a time-dependent and controlled nutrition regimen during the hormone-sensitive growth phase before first parturition can significantly affect mammary growth and subsequent lactation performance. The objective of the present study was to determine if a compensatory nutrition regimen improves lactation performance by affecting proliferation and apoptosis of mammary epithelial cells. Forty female rats (7 weeks of age, average weight 148 g) were assigned to either (1) control, free access to diet or (2) stair-step compensatory nutrition regimen, an alternating 3–4-week schedule beginning with an energy-restricted diet (31·2% restriction) for 3 weeks, followed by the control diet for 4 weeks. Estimated milk yield was greater (P <0·05) on day 15 of lactation in the compensatory nutrition group than in the control group. Mammary cell proliferation values were 1·4- and 2·7-fold greater in mammary tissue from the compensatory group during pregnant and early lactating stages respectively, compared with those from the control group. Ornithine decarboxylase (EC 4.1.1.17)mRNA was 24% higher (P <0·05) in mammary tissues of rats from the compensatory nutrition group during pregnancy than in those from the control group. These results indicate that the compensatory nutrition regimen imposed during the peripubertal growth phase stimulated mammary epithelial cell proliferation and improved lactation performance.

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