Polyunsaturated fatty acids of marine origin upregulate mitochondrial biogenesis and induce β-oxidation in white fat

Flachs, Pavel; Horakova, Olga; Brauner, Petr; Rossmeisl, Martin; Pecina, Petr; Hal, N. Franssen van; Růžičková, Jana; Sponarová, J; Drahota, Z; Vlček, Čestmı́r; Keijer, Jaap; Houštěk, J; Kopecký, Jan

doi:10.1007/s00125-005-1944-7

Cited by 338 publications

(284 citation statements)

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“…The effect in abdominal fat is associated with a 3-fold increase in the expression of genes for regulatory factors for mitochondrial biogenesis and oxidative metabolism, PPARg co-activator 1a and nuclear respiratory factor-1 respectively. A marked down-regulation of the stearoylCoA desaturase gene, Scd-1, is observed in white fat (12) , consistent with the induction of lipid oxidation by n-3 LC PUFA in the tissue (12) and the role of Scd-1 (52) in the control of lipid oxidation. Expression of PPARg coactivator 1a and nuclear respiratory factor-1 genes is also stimulated by n-3 LC PUFA in 3T3-L1 adipocytes (12) .…”

supporting

confidence: 59%

“…In particular, long-chain (LC) PUFA of the n-3 series, DHA (22: 6n-3) and EPA (20: 5n-3), which are abundant in marine fish, lower TAG while increasing HDL-cholesterol levels in plasma, prevent the development of heart disease and exert anti-inflammatory properties in human Proceedings of the Nutrition Society subjects (5)(6)(7) . Studies in rats and mice fed a high-fat or lipogenic sucrose-rich diet have shown that n-3 LC PUFA counteract the development of both obesity and insulin resistance (8)(9)(10)(11)(12)(13) . Also, in human subjects n-3 LC PUFA could reduce fat accumulation and improve glucose metabolism (14)(15)(16) .…”

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confidence: 99%

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n-3 PUFA: bioavailability and modulation of adipose tissue function

et al. 2009

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Adipose tissue has a key role in the development of metabolic syndrome (MS), which includes obesity, type 2 diabetes, dyslipidaemia, hypertension and other disorders. Systemic insulin resistance represents a major factor contributing to the development of MS in obesity. The resistance is precipitated by impaired adipose tissue glucose and lipid metabolism, linked to a low-grade inflammation of adipose tissue and secretion of pro-inflammatory adipokines. Development of MS could be delayed by lifestyle modifications, while both dietary and pharmacological interventions are required for the successful therapy of MS. The n-3 long-chain (LC) PUFA, EPA and DHA, which are abundant in marine fish, act as hypolipidaemic factors, reduce cardiac events and decrease the progression of atherosclerosis. Thus, n-3 LC PUFA represent healthy constituents of diets for patients with MS. In rodents n-3 LC PUFA prevent the development of obesity and impaired glucose tolerance. The effects of n-3 LC PUFA are mediated transcriptionally by AMP-activated protein kinase and by other mechanisms. n-3 LC PUFA activate a metabolic switch toward lipid catabolism and suppression of lipogenesis, i.e. in the liver, adipose tissue and small intestine. This metabolic switch improves dyslipidaemia and reduces ectopic deposition of lipids, resulting in improved insulin signalling. Despite a relatively low accumulation of n-3 LC PUFA in adipose tissue lipids, adipose tissue is specifically linked to the beneficial effects of n-3 LC PUFA, as indicated by (1) the prevention of adipose tissue hyperplasia and hypertrophy, (2) the induction of mitochondrial biogenesis in adipocytes, (3) the induction of adiponectin and (4) the amelioration of adipose tissue inflammation by n-3 LC PUFA.

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confidence: 59%

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confidence: 99%

n-3 PUFA: bioavailability and modulation of adipose tissue function

et al. 2009

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“…Animals and diets Experiments were performed on adult male C57BL/6J mice as described previously [1,4]. Mice were imported from the Jackson Laboratory (Bar Harbor, ME, USA) and bread at the Institute of Physiology for up to 16 generations.…”

Section: Methodsmentioning

confidence: 99%

“…Mice were killed by cervical dislocation, and subcutaneous dorsolumbar and epididymal WAT depots were dissected. Tissues were used immediately for explant studies or isolation of adipocytes [4], or stored in liquid nitrogen for RNA analysis (see below). EDTA plasma was obtained from truncal blood and stored at -70°C.…”

Section: Methodsmentioning

confidence: 99%

“…It also protected against down-regulation of solute carrier family 2 member 4 (Slc2a4, also called Glut4) in white adipose tissue (WAT) by the high-fat diet. The effect on Slc2a4 was part of a complex modulation of WAT gene expression and metabolism, resulting in stimulation of lipid oxidation and inhibition of lipogenesis, especially in the epididymal fat, which led to reduced accumulation of this tissue while food consumption remained unaffected [1,4].…”

Section: Introductionmentioning

confidence: 99%

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Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

et al. 2006

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Aims/hypothesis: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin. Methods: We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated. Results: In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA. Conclusions/interpretation: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects.

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Nutraceuticals and regulation of adipocyte life: Premises or promises

Colitti

Grasso

2014

BioFactors

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Obesity is the actual worldwide health threat, that is associated with an increased number of metabolic disorders and diseases. Following the traditional hypothesis stating that in obesity hypertrophic adipocytes trigger the adipose tissue hyperplasia, strategies to treat obesity have increased fat researches of the molecular processes that achieve adipocyte enlargement and formation that finally increase body fat mass. Moreover, a new cell type was recently identified, the "brite" adipocyte that presents a unique gene expression profile of compared to both brown and white adipocytes. Therapies against obesity, targeting these cells and their pathways, would include the induction of lipolysis and apoptosis or the inhibition of differentiation and adipogenesis. However, it should be noted that both the increase of adipocyte size and number take place in association with positive energy balance. According to the adipose tissue expansion hypothesis, adipogenesis could be related with improved metabolic health of obese people, taking back the adipose mass to a traditionally site of lipid storage. Furthermore, new perspectives in fat biology suggest that the conversion of white-to-brown adipocytes and their metabolism could be exploited for the development of therapeutic approaches against obesity-associated diseases and for the regulation of energy balance. Drugs currently available to treat obesity generally have unpleasant side effects. A novel promising approach is the usage of dietary supplements and plant products that could interfere on the life cycle of adipocyte. Here, various dietary bioactive compounds that target different stages of adipocyte life cycle and molecular and metabolic pathways are reviewed.

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Polyunsaturated fatty acids of marine origin upregulate mitochondrial biogenesis and induce β-oxidation in white fat

Cited by 338 publications

References 50 publications

n-3 PUFA: bioavailability and modulation of adipose tissue function

n-3 PUFA: bioavailability and modulation of adipose tissue function

Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet

Nutraceuticals and regulation of adipocyte life: Premises or promises

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