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- Stenblom, Eva Lena, et al.
(författare)
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Dietary thylakoids reduce visceral fat mass and increase expression of genes involved in intestinal fatty acid oxidation in high-fat fed rats
- 2016
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Ingår i: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 311:3, s. 618-627
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Tidskriftsartikel (refereegranskat)abstract
- Thylakoids reduce body weight gain and body fat accumulation in rodents. This study investigated whether an enhanced oxidation of dietary fat-derived fatty acids in the intestine contributes to the thylakoid effects. Male Sprague-Dawley rats were fed a high-fat diet with (n = 8) or without thylakoids (n = 8) for 2 wk. Body weight, food intake, and body fat were measured, and intestinal mucosa was collected and analyzed. Quantitative realtime PCR was used to measure gene expression levels of key enzymes involved in fatty acid transport, fatty acid oxidation, and ketogenesis. Another set of thylakoid-treated (n = 10) and control rats (n = 10) went through indirect calorimetry. In the first experiment, thylakoidtreated rats (n = 8) accumulated 25% less visceral fat than controls. Furthermore, fatty acid translocase (Fat/Cd36), carnitine palmitoyltransferase 1a (Cpt1a), and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2) genes were upregulated in the jejunum of the thylakoid-treated group. In the second experiment, thylakoid-treated rats (n = 10) gained 17.5% less weight compared with controls and their respiratory quotient was lower, 0.86 compared with 0.91. Thylakoid-intake resulted in decreased food intake and did not cause steatorrhea. These results suggest that thylakoids stimulated intestinal fatty acid oxidation and ketogenesis, resulting in an increased ability of the intestine to handle dietary fat. The increased fatty acid oxidation and the resulting reduction in food intake may contribute to the reduced fat accumulation in thylakoid-treated animals.
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| 2. |
- Stenkula, Karin G., et al.
(författare)
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Adipose cell size : Importance in health and disease
- 2018
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Ingår i: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 315:2, s. 284-295
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Forskningsöversikt (refereegranskat)abstract
- Adipose tissue is necessary to harbor energy. To handle excess energy, adipose tissue expands by increasing adipocyte size (hypertrophy) and number (hyperplasia). Here, we have summarized the different experimental techniques used to study adipocyte cell size and describe adipocyte size in relation to insulin resistance, type 2 diabetes, and diet interventions. Hypertrophic adipocytes have an impaired cellular function, and inherent mechanisms restrict their expansion to protect against cell breakage and subsequent inflammation. Reduction of large fat cells by diet restriction, physical activity, or bariatric surgery therefore is necessary to improve cellular function and health. Small fat cells may also be dysfunctional and unable to expand. The distribution and function of the entire cell size range of fat cells, from small to very large fat cells, are an important but understudied aspect of adipose tissue biology. To prevent dysmetabolism, therapeutic strategies to expand small fat cells, recruit new fat cells, and reduce large fat cells are needed.
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