TY - JOUR
T1 - Thylakoids reduce body fat and fat cell size by binding to dietary fat making it less available for absorption in high-fat fed mice
AU - Stenkula, Karin G.
AU - Stenblom, Eva Lena
AU - Montelius, Caroline
AU - Egecioglu, Emil
AU - Erlanson-Albertsson, Charlotte
PY - 2017/1/11
Y1 - 2017/1/11
N2 - Background: Dietary thylakoids derived from spinach have beneficial effects on body fat accumulation and blood lipids as demonstrated in humans and rodents. Important mechanisms established include delayed fat digestion in the intestine, without causing steatorrhea, and increased fatty acid oxidation in intestinal cells. The objective of our study was to elucidate if increased fecal fat excretion is an important mechanism to normalize adipose tissue metabolism during high-fat feeding in mice supplemented with thylakoids. Methods: Mice were randomized to receive HFD or thylHFD for 14 days (n = 14 for the control group and 16 for the thylakoid group). The effect of thylakoids on body fat distribution, faecal and liver fat content, and adipose tissue metabolism was investigated following high-fat feeding. Results: Thylakoid supplementation for 14 days caused an increased faecal fat content without compensatory eating compared to control. As a result, thylakoid treated animals had reduced fat mass depots and reduced liver fat accumulation compared to control. The size distribution of adipocytes isolated from visceral adipose tissue was narrowed and the cell size decreased. Adipocytes isolated from thylakoid-treated mice displayed a significantly increased lipogenesis, and protein expression of peroxisome proliferator-activated receptor gamma (PPARγ), down-stream target FAS, as well as transcription factor coactivators PGC1-α and LPIN-1 were upregulated in adipose tissue from thylakoid-fed mice. Conclusions: Together, these data suggest that thylakoid supplementation reduces body fat and fat cell size by binding to dietary fat and increasing its fecal excretion, thus reducing dietary fat available for absorption.
AB - Background: Dietary thylakoids derived from spinach have beneficial effects on body fat accumulation and blood lipids as demonstrated in humans and rodents. Important mechanisms established include delayed fat digestion in the intestine, without causing steatorrhea, and increased fatty acid oxidation in intestinal cells. The objective of our study was to elucidate if increased fecal fat excretion is an important mechanism to normalize adipose tissue metabolism during high-fat feeding in mice supplemented with thylakoids. Methods: Mice were randomized to receive HFD or thylHFD for 14 days (n = 14 for the control group and 16 for the thylakoid group). The effect of thylakoids on body fat distribution, faecal and liver fat content, and adipose tissue metabolism was investigated following high-fat feeding. Results: Thylakoid supplementation for 14 days caused an increased faecal fat content without compensatory eating compared to control. As a result, thylakoid treated animals had reduced fat mass depots and reduced liver fat accumulation compared to control. The size distribution of adipocytes isolated from visceral adipose tissue was narrowed and the cell size decreased. Adipocytes isolated from thylakoid-treated mice displayed a significantly increased lipogenesis, and protein expression of peroxisome proliferator-activated receptor gamma (PPARγ), down-stream target FAS, as well as transcription factor coactivators PGC1-α and LPIN-1 were upregulated in adipose tissue from thylakoid-fed mice. Conclusions: Together, these data suggest that thylakoid supplementation reduces body fat and fat cell size by binding to dietary fat and increasing its fecal excretion, thus reducing dietary fat available for absorption.
KW - Adipose cell size
KW - FAS
KW - Fatty liver disease
KW - PGC-1α
KW - PPARγ
UR - http://www.scopus.com/inward/record.url?scp=85010002182&partnerID=8YFLogxK
U2 - 10.1186/s12986-016-0160-4
DO - 10.1186/s12986-016-0160-4
M3 - Article
C2 - 28096887
AN - SCOPUS:85010002182
SN - 1743-7075
VL - 14
JO - Nutrition & Metabolism
JF - Nutrition & Metabolism
IS - 1
M1 - 4
ER -