title: Evidence for a major gene affecting the transition from normoglycaemia to hyperglycaemia in Psammomys obesus.
abstract: We investigated the mode of inheritance of nutritionally induced diabetes in the desert gerbil Psammomys obesus (sand rat), following transfer from low-energy (LE) to high-energy (HE) diet which induces hyperglycaemia. Psammomys selected for high or low blood glucose level were used as two parental lines. A first backcross generation (BC(1)) was formed by crossing F(1) males with females of the diabetes-prone line. The resulting 232 BC(1) progeny were assessed for blood glucose. All progeny were weaned at 3 weeks of age (week 0), and their weekly assessment of blood glucose levels proceeded until week 9 after weaning, with all progeny maintained on HE diet. At weeks 1 to 9 post weaning, a clear bimodal distribution statistically different from unimodal distribution of blood glucose was observed, normoglycaemic and hyperglycaemic at a 1:1 ratio. This ratio is expected at the first backcross generation for traits controlled by a single dominant gene. From week 0 (prior to the transfer to HE diet) till week 8, the hyperglycaemic individuals were significantly heavier (4--17%) than the normoglycaemic ones. The bimodal blood glucose distribution in BC(1) generation, with about equal frequencies in each mode, strongly suggests that a single major gene affects the transition from normo- to hyperglycaemia. The wide range of blood glucose values among the hyperglycaemic individuals (180 to 500 mg/dl) indicates that several genes and environmental factors influence the extent of hyperglycaemia. The diabetes-resistant allele appears to be dominant; the estimate for dominance ratio is 0.97.
authors.affiliation: The Robert H Smith Institute of Plant Sciences & Genetics, The Hebrew University of Jerusalem, Rehovot 76100, Israel. Hillel@agri.huji.ac.il
authors.forename: J
authors.initials: J
authors.lastname: Hillel
authors.forename: D
authors.initials: D
authors.lastname: Gefel
authors.forename: R
authors.initials: R
authors.lastname: Kalman
authors.forename: G
authors.initials: G
authors.lastname: Ben-Ari
authors.forename: L
authors.initials: L
authors.lastname: David
authors.forename: O
authors.initials: O
authors.lastname: Orion
authors.forename: M W
authors.initials: MW
authors.lastname: Feldman
authors.forename: H
authors.initials: H
authors.lastname: Bar-On
authors.forename: S
authors.initials: S
authors.lastname: Blum
authors.forename: I
authors.initials: I
authors.lastname: Raz
authors.forename: T
authors.initials: T
authors.lastname: Schaap
authors.forename: I
authors.initials: I
authors.lastname: Shpirer
authors.forename: U
authors.initials: U
authors.lastname: Lavi
authors.forename: E
authors.initials: E
authors.lastname: Shafrir
authors.forename: E
authors.initials: E
authors.lastname: Ziv
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001835:Body Weight; D003433:Crosses, Genetic; D002149:Energy Intake; D005260:Female; D005838:Genotype; D005849:Gerbillinae / Q000235:genetics*; D038321:Glycemic Index / Q000235:genetics / Q000502:physiology; D006943:Hyperglycemia / Q000235:genetics*; D008297:Male; D010641:Phenotype
chemical_list: D001786:Blood Glucose