ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Neonatal exendin-4 treatment reduces oxidative stress and prevents hepatic insulin resistance in intrauterine growth-retarded rats.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- Perinatal Semaglutide Treatment Improves Maternal Health and Mitigates Offspring Metabolic Dysfunction in a Mouse Model of Maternal Obesity.bioRxiv : the preprint server for biology · 2026Article
- Article
- The Regulation of Metabolic Homeostasis by Incretins and the Metabolic Hormones Produced by Pancreatic Islets.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Sex-specific alterations in hepatic cholesterol metabolism in low birth weight adult guinea pigs.Pediatric research · 2022Article
- Developmental origins of metabolic diseases.Physiological reviews · 2021Review
- The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism.International journal of molecular sciences · 2021Review
- Recent advances in understanding the role of glucagon-like peptide 1.F1000Research · 2020Review
- Developmental origins of nonalcoholic fatty liver disease as a risk factor for exaggerated metabolic and cardiovascular-renal disease.American journal of physiology. Endocrinology and metabolism · 2018Review
- Neuroprotective exendin-4 enhances hypothermia therapy in a model of hypoxic-ischaemic encephalopathy.Brain : a journal of neurology · 2018Article
- Oxidative Stress, Intrauterine Growth Restriction, and Developmental Programming of Type 2 Diabetes.Physiology (Bethesda, Md.) · 2018Review
- Lactational programming of glucose homeostasis: a window of opportunity.Reproduction (Cambridge, England) · 2018Review
- Glucagon-like peptide-1 ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via the PPARα pathway.Aging cell · 2018Article
- N-acetylcysteine attenuates intrauterine growth retardation-induced hepatic damage in suckling piglets by improving glutathione synthesis and cellular homeostasis.European journal of nutrition · 2018Article
- Transcriptomic Analysis Reveals Novel Mechanisms Mediating Islet Dysfunction in the Intrauterine Growth-Restricted Rat.Endocrinology · 2018Article
- Developmental and Transmittable Origins of Obesity-Associated Health Disorders.Trends in genetics : TIG · 2017Review
- Role of placental insufficiency and intrauterine growth restriction on the activation of fetal hepatic glucose production.Molecular and cellular endocrinology · 2016Article
- Glucagon-Like Peptide-1 and Its Class B G Protein-Coupled Receptors: A Long March to Therapeutic Successes.Pharmacological reviews · 2016Review
- Intrauterine Growth Restriction: Hungry for an Answer.Physiology (Bethesda, Md.) · 2016Review
- Does Glucagon-like Peptide-1 Ameliorate Oxidative Stress in Diabetes? Evidence Based on Experimental and Clinical Studies.Current diabetes reviews · 2016Review
- Effect of placental restriction and neonatal exendin-4 treatment on postnatal growth, adult body composition, and in vivo glucose metabolism in the sheep.American journal of physiology. Endocrinology and metabolism · 2015Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Intrauterine growth retardation (IUGR) has been linked to the development of type 2 diabetes in adulthood. We have developed an IUGR model in the rat whereby the animals develop diabetes later in life. Previous studies demonstrate that administration of the long-acting glucagon-like-peptide-1 agonist, exendin-4, during the neonatal period prevents the development of diabetes in IUGR rats. IUGR animals exhibit hepatic insulin resistance early in life (prior to the onset of hyperglycemia), characterized by blunted suppression of hepatic glucose production (HGP) in response to insulin. Basal HGP is also significantly higher in IUGR rats. We hypothesized that neonatal administration of exendin-4 would prevent the development of hepatic insulin resistance. IUGR and control rats were given exendin-4 on days 1-6 of life. Hyperinsulinemic-euglycemic clamp studies showed that Ex-4 significantly reduced basal HGP by 20% and normalized insulin suppression of HGP in IUGR rats. While Ex-4 decreased body weight and fat content in both Control and IUGR animals, these differences were only statistically significant in Controls. Exendin-4 prevented development of oxidative stress in liver and reversed insulin-signaling defects in vivo, thereby preventing the development of hepatic insulin resistance. Defects in glucose disposal and suppression of hepatic glucose production in response to insulin were reversed. Similar results were obtained in isolated Ex-4-treated neonatal hepatocytes. These results indicate that exposure to exendin-4 in the newborn period reverses the adverse consequences of fetal programming and prevents the development of hepatic insulin resistance.
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