Key Specifications Table
|Analytes Available||Species Reactivity||Key Applications||Detection Methods|
|Description||Rat Insulin RIA|
|Background Information||Insulin, a 5.8 kD hormone is secreted by the islet beta cells in the pancreas.|
|Detection method||Radioactive 125I|
|Linearity of Dilution||80 -100%|
|Standard Curve Range||
|Safety Information according to GHS|
|Storage and Shipping Information|
|Material Size||250 tubes|
|Protocol: Rat Insulin RIA Kit|
Rat Insulin RIA SDS
|Reference overview||Pub Med ID|
|Maternal high-fat diet programs Wnt genes through histone modification in the liver of neonatal rats.|
Ke-Feng Yang,Wei Cai,Jia-Li Xu,Wen Shi
Journal of molecular endocrinology 49 2012
Maternal high-fat (HF) diets during gestation and lactation have been shown to contribute to metabolic disorders in offspring. Molecular and epigenetic mechanisms underlying this connection may be essential for the prevention and treatment of the fetal origins of metabolic diseases. The current study examined the impact of maternal HF diets on Wnt signaling and histone modification in offspring. Time-pregnant Sprague-Dawley rats were fed either control diet or HF diet during gestation and lactation and then the neonatal offspring of both groups were investigated. The neonatal offspring born to dams fed on HF diets exhibited increases in serum glucose and liver triglyceride levels. Maternal exposure to the HF diet also repressed the mRNA expression of Wnt1 and nuclear Î²-catenin protein in the liver of offspring. The altered Wnt1 gene expression may be due to the changes of acetylation of H4 at its promoter as well as acetylation of H4 and methylation of H3K9 at coding region. Maternal exposure to the HF diet induced suppression of the Wnt/Î²-catenin signaling pathway through histone modification, potentially increasing the risk of metabolic syndrome.
|Arginine availability modulates arginine metabolism and TNFα production in peritoneal macrophages from Zucker Diabetic Fatty rats.|
Charlotte Breuillard,Linda Belabed,Sandra Bonhomme,Marie-Céline Blanc-Quintin,Nathalie Neveux,Rémy Couderc,Jean-Pascal De Bandt,Luc Cynober,Sylviane Darquy
Clinical nutrition (Edinburgh, Scotland) 31 2012
Excess weight and type 2 diabetes lead to increased susceptibility to infections. Our aim was to investigate the role of diabetes-induced decreased arginine (Arg) availability and of a possible dysregulation of Arg metabolism in macrophages favoring inflammation and dysimmunity via altered nitric oxide (NO) and cytokine productions.
|Mechanistic modeling of the effects of glucocorticoids and circadian rhythms on adipokine expression.|
Siddharth Sukumaran,William J Jusko,Debra C DuBois,Richard R Almon
The Journal of pharmacology and experimental therapeutics 337 2011
A mechanism-based model was developed to describe the effects of methylprednisolone (MPL), circadian rhythms, and the glucose/free fatty acid (FFA)/insulin system on leptin and adiponectin expression in white adipose tissue in rats. Fifty-four normal Wistar rats received 50 mg/kg MPL intramuscularly and were sacrificed at various times. An additional set of 54 normal Wistar rats were sacrificed at 18 time points across the 24-h light/dark cycle and served as controls. Measurements included plasma MPL, glucocorticoid receptor (GR) mRNA, leptin mRNA, adiponectin mRNA, plasma leptin, adiponectin, glucose, FFA, and insulin. MPL pharmacokinetics was described by a two-compartment model with two absorption components. All measured plasma markers and mRNA expression exhibited circadian patterns except for adiponectin and were described by Fourier harmonic functions. MPL caused significant down-regulation in GR mRNA with the nadir occurring at 5 h. MPL disrupted the circadian patterns in plasma glucose and FFA by stimulating their production. Plasma glucose and FFA subsequently caused an increase in plasma insulin. Furthermore, MPL disrupted the circadian patterns in leptin mRNA expression by stimulating its production. This rise was closely followed by an increase in plasma leptin. Both leptin mRNA and plasma leptin peaked at 12 h after MPL and eventually returned back to their circadian baselines. MPL and insulin had opposing effects on adiponectin mRNA expression and plasma adiponectin, which resulted in biphasic pharmacodynamic profiles. This small systems model quantitatively describes, integrates, and provides additional insights into various factors controlling adipokine gene expression.
|Different roles of zinc plus arachidonic acid on insulin sensitivity between high fructose- and high fat-fed rats.|
Inkyung Hwang,Taeho Yoon,Changhoon Kim,Byungmann Cho,Sooil Lee,Moon K Song
Life sciences 88 2011
This study was to determine the effects of zinc plus arachidonic acid (ZA) treatment on the insulin action in the specific ZA target organs using hyperinsulinemic euglycemic clamp method.
|Feeding behavior and performance of lambs are influenced by flavor diversity.|
Villalba JJ, Bach A, Ipharraguerre IR
J Anim Sci 2011
This study determined whether early experiences by sheep to the same feed, but presented in multiple or single flavors influence intake, profile of hormones involved in feed intake regulation, and the subsequent acceptability of novel feeds. Thirty-five, 2-mo-old lambs were randomly assigned to 5 treatments (7 lambs/treatment). Lambs in 1 treatment (Diversity) were fed simultaneously an unflavored control - plain ration of alfalfa and barley (75:25) and the same ration mixed (0.2%) with 1 of 3 flavors: (1) sweet, (2) umami, and (3) bitter. The other 4 treatments (Monotonous diets) received just 1 of the four rations. All animals were fed their respective rations from 0800 to 1600 for 60 d. On d 55, intake was recorded every 30 min for 8 h. On day 58 lambs were bled 1 h pre-feeding and at 30, 60, 210, 300, and 540 min post-feeding. Preference tests were conducted by offering simultaneously novel feeds of either (1) high-energy, (2) high-protein content, (3) beet pulp mixed with phytochemicals, or (4) low-quality feeds. Lambs in Diversity consumed more feed than lambs in the other treatments (P < 0.001). Lambs in Diversity consumed equivalent amounts of Plain and Umami feeds, with Umami being consumed at a greater level (P < 0.001) than the Bitter and Sweet feeds. Lambs in Diversity tended to grow faster than lambs in the other treatments (P = 0.06). On d 55, lambs in Diversity showed lower (P < 0.05) intakes than the other treatments during the 2 peaks of food consumption: 30 min and 270 min from feeding, and a trend for the lowest plasmatic concentrations of ghrelin (P = 0.06). In contrast, lambs in Diversity consumed more feed than lambs exposed to monotonous flavors at 60, 90, 120, and 180 min from feeding (P < 0.05). Lambs in Diversity also showed the lowest concentration of CCK and GLP-1 (P < 0.001). There was a trend for the greatest concentration of leptin (P = 0.14) and IGF-1 (P = 0.16) in Diversity, and for the lowest concentration of leptin in Bitter (P = 0.14). Previous experience with flavored feeds affected preference for high-energy and low-quality feeds, and for beet pulp mixed with phytochemicals (treatment x feed x day effect; P < 0.05). Thus, exposure to diverse flavors has the potential to increase feed intake and induce a more even consumption of feed across time by reducing peaks and nadirs of intake compared with exposure to monotonous rations. Flavor diversity may also influence initial acceptability and preference for novel feeds.
|Differential muscle gene expression as a function of disease progression in Goto-Kakizaki diabetic rats.|
Nie J, Xue B, Sukumaran S, Jusko WJ, Dubois DC, Almon RR
Molecular and cellular endocrinology 2011
The Goto-Kakizaki (GK) rat, a polygenic non-obese model of type 2 diabetes, is a useful surrogate for study of diabetes-related changes independent of obesity. GK rats and appropriate controls were killed at 4, 8, 12, 16 and 20 weeks post-weaning and differential muscle gene expression along with body and muscle weights, plasma hormones and lipids, and blood cell measurements were carried out. Gene expression analysis identified 204 genes showing 2-fold or greater differences between GK and controls in at least 3 ages. Array results suggested increased oxidative capacity in GK muscles, as well as differential gene expression related to insulin resistance, which was also indicated by HOMA-IR measurements. In addition, potential new biomarkers in muscle gene expression were identified that could be either a cause or consequence of T2DM. Furthermore, we demonstrate here the presence of chronic inflammation evident both systemically and in the musculature, despite the absence of obesity.Copyright © 2011. Published by Elsevier Ireland Ltd.
|Effect of high-fat diet on stress responsiveness in borderline hypertensive rats.|
Mitra A, Crump EM, Alvers KM, Robertson KL, Rowland NE
Stress 14 42-52. Epub 2010 Jul 28. 2011
Stress in combination with genetic susceptibility is a factor in the development of hypertension. We used borderline hypertensive rats to investigate whether exposure to high-fat and/or junk-food diet at different stages of ontogeny has programing consequences on stress responses. Wistar dams were fed a high- or low-fat diet for 6 weeks prior to mating with spontaneously hypertensive males, and during gestation. At birth, litters were fostered either to a dam in the same or an alternative diet condition as during gestation. After weaning, male offspring were fed either a control-chow diet or an intermittent junk food fatty diet. Between postnatal days 57-61, half of the rats in each dietary group received daily social defeat sessions using a resident-intruder protocol, and the other half were unstressed controls. Blood pressure was measured indirectly both before and after each defeat session. On the final day, rats were killed for physiological measures. Socially defeated rats showed large increases in serum corticosterone concentration and adrenal hypertrophy, indicating the effectiveness of this non-adapting stressor. Serum corticosterone level was also higher in rats fed with the junk-food diet post-weaning compared with those fed with chow only, but there were no significant effects of gestational or lactational dietary history.
|Glutamate permeability at the blood-brain barrier in insulinopenic and insulin-resistant rats.|
Hawkins RA, Mokashi A, Dejoseph MR, Vina JR, Fernstrom JD
Metabolism: clinical and experimental 59 258-266 2010
The influence of diabetes on brain glutamate (GLU) uptake was studied in insulinopenic (streptozotocin [STZ]) and insulin-resistant (diet-induced obesity [DIO]) rat models of diabetes. In the STZ study, adult male Sprague-Dawley rats were treated with STZ (65 mg/kg intravenously) or vehicle and studied 3 weeks later. The STZ rats had elevated plasma levels of glucose, ketone bodies, and branched-chain amino acids; brain uptake of GLU was very low in both STZ and control rats, examined under conditions of normal and greatly elevated (by intravenous infusion) plasma GLU concentrations. In the DIO study, rats ingested a palatable, high-energy diet for 2 weeks and were then divided into weight tertiles: rats in the heaviest tertile were designated DIO; rats in the lightest tertile, diet-resistant (DR); and rats in the intermediate tertile, controls. The DIO and DR rats continued to consume the high-energy diet for 4 more weeks, whereas the control rats were switched to standard rat chow. All rats were studied at 6 weeks (subgroups were examined under conditions of normal or elevated plasma GLU concentrations). The DIO rats ate more food and were heavier than the DR or control rats and had higher plasma leptin levels and insulin-glucose ratios. In all diet groups, the blood-brain barrier showed very low GLU penetration and was unaffected by plasma GLU concentration. Brain GLU uptake also did not differ among the diet groups. Together, the results indicate that the blood-brain barrier remains intact to the penetration of GLU in 2 models of diabetes under the conditions examined.
|Dietary intervention prior to pregnancy reverses metabolic programming in male offspring of obese rats.|
Zambrano E, Martínez-Samayoa PM, Rodríguez-González GL, Nathanielsz PW
J Physiol 588 1791-9. Epub 2010 Mar 29. 2010
Obesity involving women of reproductive years is increasing dramatically in both developing and developed nations. Maternal obesity and accompanying high energy obesogenic dietary (MO) intake prior to and throughout pregnancy and lactation program offspring physiological systems predisposing to altered carbohydrate and lipid metabolism. Whether maternal obesity-induced programming outcomes are reversible by altered dietary intake commencing before conception remains an unanswered question of physiological and clinical importance. We induced pre-pregnancy maternal obesity by feeding female rats with a high fat diet from weaning to breeding 90 days later and through pregnancy and lactation. A dietary intervention group (DINT) of MO females was transferred to normal chow 1 month before mating. Controls received normal chow throughout. Male offspring were studied. Offspring birth weights were similar. At postnatal day 21 fat mass, serum triglycerides, leptin and insulin were elevated in MO offspring and were normalized by DINT. At postnatal day 120 serum glucose, insulin and homeostasis model assessment (HOMA) were increased in MO offspring; glucose was restored, and HOMA partially reversed to normal by DINT. At postnatal day 150 fat mass was increased in MO and partially reversed in DINT. At postnatal day 150, fat cell size was increased by MO. DINT partially reversed these differences in fat cell size. We believe this is the first study showing reversibility of adverse metabolic effects of maternal obesity on offspring metabolic phenotype, and that outcomes and reversibility vary by tissue affected.
|Hyperphagia induced by sucrose: Relation to circulating and CSF glucose and corticosterone and orexigenic peptides in the arcuate nucleus.|
Gaysinskaya VA, Karatayev O, Shuluk J, Leibowitz SF
Pharmacol Biochem Behav 2010
Sucrose-rich diets compared to starch-rich diets are known to stimulate overeating under chronic conditions. The present study in normal-weight rats established an acute "preload-to-test meal" paradigm for demonstrating sucrose-induced hyperphagia and investigating possible mechanisms that mediate this behavioral phenomenon. In this acute paradigm, the rats were first given a small (15kcal) sucrose preload (30% sucrose) for 30min compared to an equicaloric, starch preload (25% starch with 5% sucrose) and then allowed to freely consume a subsequent test meal of lab chow. The sucrose preload, when compared to a starch preload equal in energy density and palatability, consistently increased food intake in the subsequent test meal occurring between 60 and 120min after the end of the preload. Measurements of hormones, metabolites and hypothalamic peptides immediately preceding this hyperphagia revealed marked differences between the sucrose vs starch groups that could contribute to the increase in food intake. Whereas the sucrose group compared to the starch group immediately after the preload (at 10min) had elevated levels of glucose in serum and cerebrospinal fluid (CSF) along with reduced expressions of neuropeptide Y (NPY) and agouti-related protein (AgRP) in the arcuate nucleus (ARC), the subsequent effects (at 30-60min) just preceding the test meal hyperphagia were the reverse. Along with lower levels of glucose, they included markedly elevated serum and CSF levels of corticosterone and mRNA levels of NPY and AgRP in the ARC. In addition to establishing an animal model for sucrose-induced hyperphagia, these results demonstrate peripheral and central mechanisms that may mediate this behavioral phenomenon.
|Quality Control Ranges for Catalog # 6000-K Expected Ranges of Each Analyte Using EMD MILLIPORE RIA Kits as Listed Below|
|Full Service Custom-built Assays (MilliporeSigma)|