title: Carbohydrate- and lipid-enriched meals acutely disrupt glycemic homeostasis by inducing transient insulin resistance in rats.
abstract: Chronic intake of high-carbohydrate or high-lipid diets is a well-known insulin resistance inducer. This study investigates the immediate effect (1-6 h) of a carbohydrate- or lipid-enriched meal on insulin sensitivity. Fasted rats were refed with standard, carbohydrate-enriched (C), or lipid-enriched (L) meal. Plasma insulin, glucose, and non-esterified fatty acids (NEFA) were measured at 1, 2, 4, and 6 h of refeeding. The glucose-insulin index showed that either carbohydrates or lipids decreased insulin sensitivity at 2 h of refeeding. At this time point, insulin tolerance tests (ITTs) and glucose tolerance tests (GTTs) detected insulin resistance in C rats, while GTT confirmed it in L rats. Reduced glycogen and phosphorylated AKT and GSK3 content revealed hepatic insulin resistance in C rats. Reduced glucose uptake in skeletal muscle subjected to the fatty acid concentration that mimics the high NEFA level of L rats suggests insulin resistance in these animals is mainly in muscle. In conclusion, carbohydrate- or lipid-enriched meals acutely disrupt glycemic homeostasis, inducing a transient insulin resistance, which seems to involve liver and skeletal muscle, respectively. Thus, the insulin resistance observed when those types of diets are chronically consumed may be an evolution of repeated episodes of this transient insulin resistance.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Brazil. raqscamp@icb.usp.br
authors.forename: Raquel Saldanha
authors.initials: RS
authors.lastname: Campello
authors.forename: Ana Barbara Teixeira
authors.initials: AB
authors.lastname: Alves-Wagner
authors.forename: Fernando
authors.initials: F
authors.lastname: Abdulkader
authors.forename: Rosana Cristina Tieko
authors.initials: RC
authors.lastname: Mori
authors.forename: Ubiratan Fabres
authors.initials: UF
authors.lastname: Machado
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D003847:Deoxyglucose / Q000378:metabolism; D059305:Diet, High-Fat; D004040:Dietary Carbohydrates / Q000008:administration & dosage* / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage* / Q000378:metabolism; D005215:Fasting / Q000097:blood / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005951:Glucose Tolerance Test / Q000379:methods; D038321:Glycemic Index; D006003:Glycogen / Q000378:metabolism; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D006706:Homeostasis; D007328:Insulin / Q000097:blood* / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004268:DNA-Binding Proteins; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; C506347:GLUT4 enhancer factor, rat; D007328:Insulin; D014157:Transcription Factors; D006003:Glycogen; D003847:Deoxyglucose; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3