RGD Reference Report - Glucose metabolism and insulin sensitivity in transgenic mice overexpressing leptin with lethal yellow agouti mutation: usefulness of leptin for the treatment of obesity-associated diabetes. - Rat Genome Database

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Glucose metabolism and insulin sensitivity in transgenic mice overexpressing leptin with lethal yellow agouti mutation: usefulness of leptin for the treatment of obesity-associated diabetes.

Authors: Masuzaki, H  Ogawa, Y  Aizawa-Abe, M  Hosoda, K  Suga, J  Ebihara, K  Satoh, N  Iwai, H  Inoue, G  Nishimura, H  Yoshimasa, Y  Nakao, K 
Citation: Masuzaki H, etal., Diabetes. 1999 Aug;48(8):1615-22.
RGD ID: 2314006
Pubmed: PMID:10426381   (View Abstract at PubMed)

Leptin acts as an adipocyte-derived blood-borne satiety factor that can increase glucose metabolism. To elucidate the therapeutic implications of leptin for obesity-associated diabetes, we crossed transgenic skinny mice overexpressing leptin (Tg/+), which we have developed recently, and lethal yellow KKAy mice (Ay/+), a genetic model for obesity-diabetes syndrome, and examined the metabolic phenotypes of F1 animals. At 6 weeks of age, plasma leptin concentrations in Tg/+ mice with the Ay allele (Tg/+:Ay/+) were significantly higher than those in Ay/+ mice. Although no significant differences in body weight were noted among Tg/+:Ay/+ mice, Ay/+ mice, and their wild-type lean littermates (+/+), glucose and insulin tolerance tests revealed increased glucose tolerance and insulin sensitivity in Tg/+:Ay/+ compared with Ay/+ mice. However, at 12 weeks of age, when plasma leptin concentrations in Ay/+ mice were comparable to those in Tg/+:Ay/+ mice, Tg/+:Ay/+ mice developed obesity-diabetes syndrome similar to that of Ay/+ mice. Body weights of 12-week-old Tg/+:Ay/+ and Ay/+ mice were reduced to those of +/+ mice by a 3-week food restriction; when plasma leptin concentrations remained high in Tg/+:Ay/+ mice but were markedly reduced in Ay/+ and +/+ mice, glucose tolerance and insulin sensitivity in Tg/+:Ay/+ mice were markedly improved as compared with Ay/+ and +/+ mice. The present study demonstrates that hyperleptinemia can delay the onset of impaired glucose metabolism and accelerate the recovery from diabetes during caloric restriction in Tg/+:Ay/+ mice, thereby suggesting the potential usefulness of leptin in combination with a long-term caloric restriction for the treatment of obesity-associated diabetes.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ASIPHumandiabetes mellitus  ISOa (Mus musculus)associated with Obesity and DNA:mutation (mouse)RGD 
AsipRatdiabetes mellitus  ISOa (Mus musculus)associated with Obesity and DNA:mutation (mouse)RGD 
aMousediabetes mellitus  IAGP associated with Obesity and DNA:mutation (mouse)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Asip  (agouti signaling protein)

Genes (Mus musculus)
a  (non-agouti)

Genes (Homo sapiens)
ASIP  (agouti signaling protein)


Additional Information