Abstract
The allograft inflammatory factor (AIF) gene family consists of two identified paralogs – AIF1 and AIF1-like (AIF1L). The encoded proteins, AIF1 and AIF1L, are 80% similar in sequence and show conserved tertiary structure. While studies in human populations suggest links between AIF1 and metabolic diseases such as obesity and diabetes, such associations with AIF1L have not been reported. Drawing parallels based on structural similarity, we postulated that AIF1L might contribute to metabolic disorders, and studied it using mouse models. Here we report that AIF1L is expressed in major adipose depots and kidney but was not detectable in liver or skeletal muscle; in notable contrast to AIF1, AIF1L was also not found in spleen. Studies of AIF1L deficient mice showed no obvious postnatal developmental phenotype. In response to high fat diet (HFD) feeding for 6 or 18 weeks, WT and AIF1L deficient mice gained weight similarly, showed no differences in fat or lean mass accumulation, and displayed no changes in energy expenditure or systemic glucose handling. These findings indicate that AIF1L is not essential for the development of obesity or impaired glucose handling due to HFD, and advance understanding of this little-studied gene and its place in the AIF gene family.
Highlights
The allograft inflammatory factor (AIF) gene family consists of two identified paralogs – AIF1 and AIF1like (AIF1L)
We report that AIF1L expression in mice is detectable in the 3 major adipose depots – BAT, SAT, and epididymal white adipose tissue (eWAT) – and in kidney, lung, and brain
Using a genetic deletion in the mouse, we found that loss of AIF1L did not affect (1) embryonic development, (2) growth and maintenance of body weight from postnatal stage (5 weeks) to adult stage (8 weeks), (3) body composition or adiposity, (4) energy expenditure, or (5) glucose sensitivity
Summary
The allograft inflammatory factor (AIF) gene family consists of two identified paralogs – AIF1 and AIF1like (AIF1L). While studies in human populations suggest links between AIF1 and metabolic diseases such as obesity and diabetes, such associations with AIF1L have not been reported. In response to high fat diet (HFD) feeding for 6 or 18 weeks, WT and AIF1L deficient mice gained weight showed no differences in fat or lean mass accumulation, and displayed no changes in energy expenditure or systemic glucose handling. These findings indicate that AIF1L is not essential for the development of obesity or impaired glucose handling due to HFD, and advance understanding of this little-studied gene and its place in the AIF gene family. Obesity is either associated with or poses an independent risk for the development of several pathophysiological conditions such as cancer[11], cardiovascular diseases[12], and non-alcoholic-fatty liver disease[13]
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