Omega‐3 PUFA of marine origin limit diet‐induced obesity in mice by reducing cellularity of adipose tissue

Růžičková, Jana; Rossmeisl, Martin; Prazak, Tomas; Flachs, Pavel; Sponarová, J; Vecka, Marek; Tvrzická, E; Bryhn, Morten; Kopecký, Jan

doi:10.1007/s11745-004-1345-9

Cited by 270 publications

(265 citation statements)

References 35 publications

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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%

“…a composite high-fat diet, but with partial replacement of lipids by fish oil concentrate (cHF-F1 diet) such that 15% (wt/wt) of lipids was replaced by the EPA/DHA concentrate containing 6% EPA, 51% DHA, and 4 mg/g α-tocopherol as antioxidant (EPAX 1050TG; Pronova Biocare, Lysaker, Norway). Detailed analysis of fatty acid composition of the diets was performed previously [1]. When indicated, the ration was reduced by 30% (caloric restriction) compared with mice on the same type of diet but with free access to chow.…”

Section: Methodsmentioning

confidence: 99%

“…EPA and DHA act as hypolipidaemics, exert prophylactic effects on cardiovascular disease, protect against insulin resistance and obesity in rodents fed high-fat diets, and reduce insulin response to glucose in healthy humans [1-3 and references therein]. We, and others, have shown [1] that in a semi-synthetic high-fat diet rich in α-linolenic acid (18:3 n-3) partial replacement of lipids with concentrate of EPA and DHA from sea fish (EPA/DHA) resulted in suppression of insulinaemia. 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.…”

Section: Introductionmentioning

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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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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“…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) .…”

mentioning

confidence: 99%

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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Lipids, Brain, and Mental Health

Hussain

Rasul

Anwar

et al. 2020

Bailey's Industrial Oil and Fat Products

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Lipids in nervous system are of particular interest because of the high concentration of lipids in brain, second only to adipose tissue, of which a major part is found in myelin. These lipids are involved in the structure of cell membranes in the brain and display a variety of biological functions to maintain vital cellular processes at various levels: work as energy source, serve as signaling molecules, and withstand structural integrity of cellular compartment and membranes. Lipids in the form of fatty acids participate actively in the development of the nervous system at embryonic and early postnatal stage and are crucial for its maintenance throughout adulthood. The involvement of deregulated metabolism of lipids in many nervous system disorders, pathological conditions and injuries underscores the importance of lipids in maintaining normal cell signaling and tissue physiology. The correction of altered lipid levels by exogenous supply is considered as a most promising therapeutic approach. It is believed that they contribute in their own right by as yet incompletely understood mechanisms to those pathological processes. This article attempts to provide an overview of the lipid imbalances associated with CNS injury (traumatic brain injury, stroke, and spinal cord injury), neurological disorders (schizophrenia, anxiety, and depressive illnesses), and neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, and multiple sclerosis). Fatty acids as biomarkers of diseases are briefly discussed as well as their therapeutic potential which will provide new insights to exploit these lipids to open new avenues for improving brain health, prevention, and treatment of nervous system disorders.

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Omega‐3 PUFA of marine origin limit diet‐induced obesity in mice by reducing cellularity of adipose tissue

Cited by 270 publications

References 35 publications

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

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

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

Lipids, Brain, and Mental Health

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