Disparate metabolic response to fructose feeding between different mouse strains
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Disparate metabolic response to fructose feeding between different mouse strains. / Montgomery, M. K.; Fiveash, C. E.; Braude, J. P.; Osborne, B.; Brown, S. H.J.; Mitchell, T. W.; Turner, N.
In: Scientific Reports, Vol. 5, 18474, 22.12.2015.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Disparate metabolic response to fructose feeding between different mouse strains
AU - Montgomery, M. K.
AU - Fiveash, C. E.
AU - Braude, J. P.
AU - Osborne, B.
AU - Brown, S. H.J.
AU - Mitchell, T. W.
AU - Turner, N.
PY - 2015/12/22
Y1 - 2015/12/22
N2 - Diets enriched in fructose (FR) increase lipogenesis in the liver, leading to hepatic lipid accumulation and the development of insulin resistance. Previously, we have shown that in contrast to other mouse strains, BALB/c mice are resistant to high fat diet-induced metabolic deterioration, potentially due to a lack of ectopic lipid accumulation in the liver. In this study we have compared the metabolic response of BALB/c and C57BL/6 (BL6) mice to a fructose-enriched diet. Both strains of mice increased adiposity in response to FR-feeding, while only BL6 mice displayed elevated hepatic triglyceride (TAG) accumulation and glucose intolerance. The lack of hepatic TAG accumulation in BALB/c mice appeared to be linked to an altered balance between lipogenic and lipolytic pathways, while the protection from fructose-induced glucose intolerance in this strain was likely related to low levels of ER stress, a slight elevation in insulin levels and an altered profile of diacylglycerol species in the liver. Collectively these findings highlight the multifactorial nature of metabolic defects that develop in response to changes in the intake of specific nutrients and the divergent response of different mouse strains to dietary challenges.
AB - Diets enriched in fructose (FR) increase lipogenesis in the liver, leading to hepatic lipid accumulation and the development of insulin resistance. Previously, we have shown that in contrast to other mouse strains, BALB/c mice are resistant to high fat diet-induced metabolic deterioration, potentially due to a lack of ectopic lipid accumulation in the liver. In this study we have compared the metabolic response of BALB/c and C57BL/6 (BL6) mice to a fructose-enriched diet. Both strains of mice increased adiposity in response to FR-feeding, while only BL6 mice displayed elevated hepatic triglyceride (TAG) accumulation and glucose intolerance. The lack of hepatic TAG accumulation in BALB/c mice appeared to be linked to an altered balance between lipogenic and lipolytic pathways, while the protection from fructose-induced glucose intolerance in this strain was likely related to low levels of ER stress, a slight elevation in insulin levels and an altered profile of diacylglycerol species in the liver. Collectively these findings highlight the multifactorial nature of metabolic defects that develop in response to changes in the intake of specific nutrients and the divergent response of different mouse strains to dietary challenges.
UR - http://www.scopus.com/inward/record.url?scp=84951325501&partnerID=8YFLogxK
U2 - 10.1038/srep18474
DO - 10.1038/srep18474
M3 - Journal article
C2 - 26690387
AN - SCOPUS:84951325501
VL - 5
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 18474
ER -
ID: 357521802