TY - JOUR
T1 - Allograft inflammatory factor-1-like is not essential for age dependent weight gain or HFD-induced obesity and glucose insensitivity
AU - Parikh, Dippal
AU - Riascos-Bernal, Dario F.
AU - Egaña-Gorroño, Lander
AU - Jayakumar, Smitha
AU - Almonte, Vanessa
AU - Chinnasamy, Prameladevi
AU - Sibinga, Nicholas E.S.
N1 - Funding Information:
We would like to thank the Einstein Diabetes Center Animal Physiology core facility for assistance with performing Echo-MRI, CT Scans, and metabolic cage studies. We would also like to thank the histopathology core facility and biomarker analytic research core (BARC) Einstein for help with H&E staining and serum analyte measurements respectively. These studies were supported by NIH grant R01HL128066 to N.E.S.S.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/12/1
Y1 - 2020/12/1
N2 - 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.
AB - 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.
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U2 - 10.1038/s41598-020-60433-4
DO - 10.1038/s41598-020-60433-4
M3 - Article
C2 - 32107417
AN - SCOPUS:85080974018
SN - 2045-2322
VL - 10
JO - Scientific reports
JF - Scientific reports
IS - 1
M1 - 3594
ER -
