Thylakoids reduce body fat and fat cell size by binding to dietary fat making it less available for absorption in high-f
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RESEARCH
Open Access
Thylakoids reduce body fat and fat cell size by binding to dietary fat making it less available for absorption in high-fat fed mice Karin G. Stenkula1*, Eva-Lena Stenblom2, Caroline Montelius2, Emil Egecioglu2 and Charlotte Erlanson-Albertsson2
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. Keywords: PPARγ, PGC-1α, FAS, Adipose cell size, Fatty liver disease
Background Obesity is characterized by an excess fat mass due to chronic imbalance between energy intake and energy expenditure. Several comorbidities are associated with obesity, such as diabetes, cardiovascular disease and non-alcoholic fatty-liver disease (NAFLD). These comorbidities increase in prevalence at a high rate, underscoring an urgent need for strategies to prevent the emerging global epidemic [1]. * Correspondence: [email protected] 1 Glucose Transport and Protein Trafficking, Department of Experimental Medical Science, BMC, Lund University, 221 84 Lund, Sweden Full list of author information is available at the end of the article
An overload of energy in the form of dietary fat plays a significant role in promoting obesity compared to protein and carbohydrate [2]. Weight loss can therefore be achieved by reducing the consumption of fat or the absorption of fat. Lipase inhibitors are efficient in reducing body weight, however often with apparent ga
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