title: Thylakoids reduce body fat and fat cell size by binding to dietary fat making it less available for absorption in high-fat fed mice.
abstract: 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.
authors.affiliation: Glucose Transport and Protein Trafficking, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden.
authors.forename: Karin G
authors.initials: KG
authors.lastname: Stenkula
authors.affiliation: Appetite Control, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden.
authors.forename: Eva-Lena
authors.initials: EL
authors.lastname: Stenblom
authors.affiliation: Appetite Control, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden.
authors.forename: Caroline
authors.initials: C
authors.lastname: Montelius
authors.affiliation: Appetite Control, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden.
authors.forename: Emil
authors.initials: E
authors.lastname: Egecioglu
authors.affiliation: Appetite Control, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden.
authors.forename: Charlotte
authors.initials: C
authors.lastname: Erlanson-Albertsson
keywords: Adipose cell size; FAS; Fatty liver disease; PGC-1α; PPARγ