Dietary supplementation with ω-3 PUFA increases adiponectin and attenuates ventricular remodeling and dysfunction with pressure overload

Duda, Monika; O’Shea, Karen M.; Lei, Biao; Barrows, Brian R.; Azimzadeh, Agnes M.; McElfresh, Tracy E.; Hoit, Brian D.; Kop, Willem J.; Stanley, William C.

doi:10.1016/j.cardiores.2007.07.002

Cited by 100 publications

(100 citation statements)

References 34 publications

(51 reference statements)

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“…This resulted in attenuation of left ventricular remodeling and dysfunction. 85,117,118 In a subsequent study, a linoleateenriched high-fat diet (but not saturated high-fat diet) attenuated cardiac hypertrophy, left ventricular chamber dilation, and improved systolic function in aged hypertensive heart failure rats. 119 Moreover, a high-fat diet reduced cardiac hypertrophy and improved contractile function in Dahl salt-sensitive rats.…”

Section: Approaches To Treat Left Heart Failure Inhibiting Fat Oxidationmentioning

confidence: 94%

Cardiac Energy Metabolic Alterations in Pressure Overload–Induced Left and Right Heart Failure (2013 Grover Conference Series)

Sankaralingam

Lopaschuk

2015

Pulm. circ.

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Pressure overload of the heart, such as seen with pulmonary hypertension and/or systemic hypertension, can result in cardiac hypertrophy and the eventual development of heart failure. The development of hypertrophy and heart failure is accompanied by numerous molecular changes in the heart, including alterations in cardiac energy metabolism. Under normal conditions, the high energy (adenosine triphosphate [ATP]) demands of the heart are primarily provided by the mitochondrial oxidation of fatty acids, carbohydrates (glucose and lactate), and ketones. In contrast, the hypertrophied failing heart is energy deficient because of its inability to produce adequate amounts of ATP. This can be attributed to a reduction in mitochondrial oxidative metabolism, with the heart becoming more reliant on glycolysis as a source of ATP production. If glycolysis is uncoupled from glucose oxidation, a decrease in cardiac efficiency can occur, which can contribute to the severity of heart failure due to pressure-overload hypertrophy. These metabolic changes are accompanied by alterations in the enzymes that are involved in the regulation of fatty acid and carbohydrate metabolism. It is now becoming clear that optimizing both energy production and the source of energy production are potential targets for pharmacological intervention aimed at improving cardiac function in the hypertrophied failing heart. In this review, we will focus on what alterations in energy metabolism occur in pressure overload induced left and right heart failure. We will also discuss potential targets and pharmacological approaches that can be used to treat heart failure occurring secondary to pulmonary hypertension and/or systemic hypertension.

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Section: Approaches To Treat Left Heart Failure Inhibiting Fat Oxidationmentioning

confidence: 94%

Cardiac Energy Metabolic Alterations in Pressure Overload–Induced Left and Right Heart Failure (2013 Grover Conference Series)

Sankaralingam

Lopaschuk

2015

Pulm. circ.

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“…fluence cardiac remodeling [11,12]. Low levels of adiponectin are associated with a further progression of left ventricular hypertrophy in patients presenting with hypertension, left ventricular diastolic dysfunction, and hypertrophy [13].…”

mentioning

confidence: 99%

“…Because acromegaly is also a systemic disorder characterized by morbidities similar to those of a metabolic syndrome, hypoadiponectinemia may be involved in the pathogenesis of insulin resistance and related metabolic disorders as well as cardiac changes present in active acromegaly [10][11][12][13][14][15][16][17]. Indeed, adiponectin levels in acromegalic patients have been reported variably as higher than [18] or similar to [19,20] those in normal controls.…”

mentioning

confidence: 99%

Adiponectin and Cardiac Hypertrophy in Acromegaly

Gurbulak¹,

Akın²,

Yerlikaya³

et al. 2016

Adv Clin Exp Med

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“…They established that dietary fish oil reversed the inhibitory effects of a long-term sucroserich diet on serum leptin and total adiponectin levels [53] . Since then, many studies have confirmed that dietary fish oils and omega-3 fatty acids increase total adiponectin concentrations [54,56,[105][106][107][108] . Sneddon and colleagues examined the effects of CLA and omega-3 fatty acids on plasma leptin and adiponectin concentrations [55] .…”

Section: Adiponectinmentioning

confidence: 97%

Pharmacological effects of lipid-lowering drugs on circulating adipokines

Wanders

Plaisance²,

Judd³

2010

WJD

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The cardioprotective effects of lipid-lowering drugs have been primarily attributed to their effects on blood lipid metabolism. However, emerging evidence indicates that lipid-lowering drugs also modulate the synthesis and secretion of adipose tissue-secreted proteins referred to as adipokines. Adipokines influence energy homeostasis and metabolism and have also been shown to modulate the vascular inflammatory cascade. The purpose of this review will be to examine the reported effects of commonly used lipid-lowering drugs (statins, fibrates, niacin and omega-3-fatty acids) on the circulating concentrations of leptin, adiponectin, tumor necrosisfactor-α (TNF-α), Retinol binding protein 4 (RBP4) and resistin. Overall, the lipid-lowering drugs reviewed have minimal effects on leptin and resistin concentrations. Conversely, circulating adiponectin concentrations are consistently increased by each lipid-lowering drug reviewed with the greatest effects produced by niacin. Studies that have examined the effects of statins, niacin and omega-3-fatty acids on TNF-α demonstrate that these agents have little effect on circulating TNF-α concentrations. Niacin and fibrates appear to lower RBP4 but not resistin concentrations. The results of the available studies suggest that a strong relationship exists between pharmacological reductions in blood lipids and adiponectin that is not obvious for other adipokines reviewed.

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Dietary supplementation with ω-3 PUFA increases adiponectin and attenuates ventricular remodeling and dysfunction with pressure overload

Abstract: Dietary supplementation with omega-3 PUFA attenuated pressure overload-induced LV dysfunction, which was associated with elevated plasma adiponectin.

Cited by 100 publications

References 34 publications

Cardiac Energy Metabolic Alterations in Pressure Overload–Induced Left and Right Heart Failure (2013 Grover Conference Series)

Cardiac Energy Metabolic Alterations in Pressure Overload–Induced Left and Right Heart Failure (2013 Grover Conference Series)

Adiponectin and Cardiac Hypertrophy in Acromegaly

Pharmacological effects of lipid-lowering drugs on circulating adipokines

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