Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq-/- or Adipo-/-) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis.
At The Jackson Laboratory, it is our experience that breeding Adipoqtm1Chan homozygous mice together frequently results in pups with significant hair loss by wean age (3 weeks). It is not determined if this phenotype is caused by the genotype of the pups, or if the phenotype is imparted upon the pups due to the genotype of the lactating/nursing female. In most cases, the hair loss phenotype is reversed after weaning, with some pups growing a full coat by 6 weeks of age.
