title: Evaluation of genetic predisposition to insulin resistance by nutrient-induced insulin output ratio (NIOR).
abstract: BACKGROUND
  New tools to identify genotype-phenotype interactions need to be described and implemented. The aim of this study was to identify correlation between the risk originating from gene variation and diet-dependent development of insulin resistance.
  
  
  METHODS
  Insulin output in terms of area under the curve after an oral glucose tolerance test (AUC Ins OGTT) and lipid tolerance tests (AUC Ins OLTT) were measured in 167 overweight/obese patients. Estimation of the 18 common gene polymorphisms for obesity risk and standard phenotyping were performed.
  
  
  RESULTS
  Insulin output (AUC Ins OGTT) correlated strongly between both insulin treatments across the whole group. However, within the genotype sub-groups, correlation was lower or did not exist. Using a nutrient-induced insulin output ratio (NIOR), calculated as AUC Ins OLTT/AUC Ins OGTT, values ranged from 0.42 to 5.83 and correlated significantly with body mass index (BMI) and leptin, but not with age, gender, waist-to-hip ratio (WHR) and homeostasis model assessment of insulin resistance (HOMA-IR) or plasma adiponectin. High NIOR was found in a subgroup of carriers of rare allelic variants of genes characteristic for poorer tolerance to lipids in the diet. Low NIOR values were found within a sub-group with rare genetic variants regulating carbohydrate metabolism. Thus, the new insulin index NIOR may distinguish gene variant carriers into groups of glucose- or lipid-sensitive phenotypes.
  
  
  CONCLUSIONS
  We suggest that the OLTT/OGTT insulin output ratio (NIOR) may be predictive for identifying individuals who are phenotypically susceptible to insulin resistance in response to high fat or carbohydrate in their habitual diet.
authors.affiliation: Department of Clinical Biochemistry, The Jagiellonian University, Medical College, Krakow, Poland. mbwybran@cyf-kr.edu.pl
authors.forename: Iwona
authors.initials: I
authors.lastname: Wybranska
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Malczewska-Malec
authors.forename: Lukasz
authors.initials: L
authors.lastname: Partyka
authors.forename: Beata
authors.initials: B
authors.lastname: Kiec-Wilk
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Kosno
authors.forename: Iwona
authors.initials: I
authors.lastname: Leszczynska-Golabek
authors.forename: Anna
authors.initials: A
authors.lastname: Zdzienicka
authors.forename: Anna
authors.initials: A
authors.lastname: Gruca
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Kwasniak
authors.forename: Aldona
authors.initials: A
authors.lastname: Dembinska-Kiec
mesh_terms: D000328:Adult; D019540:Area Under Curve; D015992:Body Mass Index; D005260:Female; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D054439:Ghrelin / Q000235:genetics* / Q000502:physiology; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D008055:Lipids / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009765:Obesity; D011110:Polymorphism, Genetic
chemical_list: D054439:Ghrelin; D007328:Insulin; D008055:Lipids