Recessive mutations at the rat fatty locus (fa, fa(cp)), which produce
obesity, insulin resistance, and diabetes, provide useful experimenta
l models for similar phenotypes in humans, The molecular pathogenesis
of the metabolic phenotype in animals segregating for fa is unknown an
d difficult to study once the confounding metabolic effects of obesity
are present. Although various experimental methods distinguish preobe
se from lean rats (phenotypic markers and molecular markers geneticall
y linked 60 fatty), technical difficulties limit their utility, We rep
ort the identification of two (GT)(n) simple sequence repeats (SSRs) n
ear the rat phosphoglucomutase gene (Pgm1) gene and two SSRs, (GA)(n)
and (GT)(n), near the rat complement component 8 beta gene (C8b). Thes
e SSRs map to an similar to 4-cM interval flanking the fatty locus on
rat chromosome 5, Use of these molecular markers in combination offers
an improved method for early assessment of gene dosage for fa and hen
ce for studying the fundamental molecular physiology underlying the de
rangements of metabolism and behavior resulting from mutations in this
gene. (C) 1995 Academic Press, Inc.