scholarly journals The passive coping Roman Low Avoidance rat, a non-obese rat model for insulin resistance

2009 ◽  
Vol 97 (3-4) ◽  
pp. 353-358 ◽  
Author(s):  
G.J. Boersma ◽  
A.J.W. Scheurink ◽  
P.Y. Wielinga ◽  
T.J. Steimer ◽  
L. Benthem
Keyword(s):  
Insulin Resistance ◽  
Rat Model ◽  
Passive Coping ◽  
Roman Low Avoidance

Cacao extract enriched in polyphenols prevents insulin-resistance and dyslipemia in a rat model

2017 ◽  
Author(s):  
JL Rios ◽  
H Villagarcía ◽  
C Castro María ◽  
L González Arbeláez ◽  
L Massa María ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Rat Model

scholarly journals Sympathetic nervous dysregulation in the absence of systolic left ventricular dysfunction in a rat model of insulin resistance with hyperglycemia

2011 ◽  
Vol 10 (1) ◽  
pp. 75 ◽  
Author(s):  
James T Thackeray ◽  
Jerry Radziuk ◽  
Mary-Ellen Harper ◽  
Erik J Suuronen ◽  
Kathryn J Ascah ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Left Ventricular Dysfunction ◽  
Rat Model ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Sympathetic Nervous

scholarly journals Insulin resistance in penile arteries from a rat model of metabolic syndrome

2010 ◽  
Vol 161 (2) ◽  
pp. 350-364 ◽  
Author(s):  
Cristina Contreras ◽  
Ana Sánchez ◽  
Pilar Martínez ◽  
Rafaela Raposo ◽  
Belén Climent ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Rat Model ◽  
Penile Arteries

scholarly journals Hyperandrogenism and Insulin Resistance, Not Changes in Body Weight, Mediate the Development of Endothelial Dysfunction in a Female Rat Model of Polycystic Ovary Syndrome (PCOS)

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4071-4080 ◽  
Author(s):  
Amanda Hurliman ◽  
Jennifer Keller Brown ◽  
Nicole Maille ◽  
Maurizio Mandala ◽  
Peter Casson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Polycystic Ovary Syndrome ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Phase 1 ◽  
Ovary Syndrome

This study was designed to differentiate the contributions of hyperandrogenism, insulin resistance (IR), and body weight to the development of endothelial dysfunction in polycystic ovary syndrome and determine the effectiveness of insulin sensitization and antiandrogenic therapy after the establishment of vascular and metabolic dysfunction using a rat model of polycystic ovary syndrome. We hypothesized that the observed endothelial dysfunction was a direct steroidal effect, as opposed to changes in insulin sensitivity or body weight. Prepubertal female rats were randomized to the implantation of a pellet containing DHT or sham procedure. In phase 1, DHT-exposed animals were randomized to pair feeding to prevent weight gain or metformin, an insulin-sensitizing agent, from 5 to 14 weeks. In phase 2, DHT-exposed animals were randomized to treatment with metformin or flutamide, a nonsteroidal androgen receptor blocker from 12 to 16 weeks. Endothelial function was assessed by the vasodilatory response of preconstricted arteries to acetylcholine. Serum steroid levels were analyzed in phase 1 animals. Fasting blood glucose and plasma insulin were analyzed and homeostasis model assessment index calculated in all animals. Our data confirm the presence of endothelial dysfunction as well as increased body weight, hypertension, hyperinsulinemia, and greater IR among DHT-treated animals. Even when normal weight was maintained through pair feeding, endothelial dysfunction, hyperinsulinemia, and IR still developed. Furthermore, despite weight gain, treatment with metformin and flutamide improved insulin sensitivity and blood pressure and restored normal endothelial function. Therefore, the observed endothelial dysfunction is most likely a direct result of hyperandrogenism-induced reductions in insulin sensitivity, as opposed to weight gain.

Blockade of sensory abnormalities and kinin B1 receptor expression by N-Acetyl-l-Cysteine and ramipril in a rat model of insulin resistance

2008 ◽  
Vol 589 (1-3) ◽  
pp. 66-72 ◽  
Author(s):  
Mahmoud Ali Ismael ◽  
Sébastien Talbot ◽  
Cynthia L. Carbonneau ◽  
Christian M. Beauséjour ◽  
Réjean Couture
Keyword(s):  
Insulin Resistance ◽  
Rat Model ◽  
Receptor Expression ◽  
Sensory Abnormalities ◽  
B1 Receptor ◽  
Kinin B1 Receptor

Insulin sensitivity, leptin, adiponectin, resistin, and testosterone in adult male and female rats after maternal-neonatal separation and environmental stress

2018 ◽  
Vol 314 (1) ◽  
pp. R12-R21 ◽  
Author(s):  
Hershel Raff ◽  
Brian Hoeynck ◽  
Mack Jablonski ◽  
Cole Leonovicz ◽  
Jonathan M. Phillips ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adult Male ◽  
Rat Model ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Neonatal Hypoxia ◽  
Male And Female Rats ◽  
Plasma Leptin ◽  
Neonatal Separation

Care of premature infants often requires parental and caregiver separation, particularly during hypoxic and hypothermic episodes. We have established a neonatal rat model of human prematurity involving maternal-neonatal separation and hypoxia with spontaneous hypothermia prevented by external heat. Adults previously exposed to these neonatal stressors show a sex difference in the insulin and glucose response to arginine stimulation suggesting a state of insulin resistance. The current study used this cohort of adult rats to evaluate insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and testosterone. The major findings were that daily maternal-neonatal separation led to an increase in body weight and HOMA-IR in adult male and female rats and increased plasma leptin in adult male rats only; neither prior neonatal hypoxia (without or with body temperature control) nor neonatal hypothermia altered subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; male-female differences in resistin were lost in the adults that were exposed to hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone in adult male rats. We conclude that neonatal stressors result in subsequent adult sex-dependent increases in insulin resistance and adipokines and that our rat model of prematurity with hypoxia without hypothermia alters adult testosterone dynamics.

Desaturase activities in rat model of insulin resistance induced by a sucrose-rich diet

Lipids ◽  
2003 ◽  
Vol 38 (7) ◽  
pp. 733-742 ◽  
Author(s):  
Rodolfo R. Brenner ◽  
Omar J. Rimoldi ◽  
Yolanda B. Lombardo ◽  
María S. González ◽  
Ana M. Bernasconi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Rat Model
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