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Omega-3 polyunsaturated fatty acid enriched diet attenuates stress-induced lactacidemia in 10-day-old rats
M Skalski1, M Goto, T Ravindranath
1The Ronald McDonald Children's Hospital at Loyola, Illinois, USA.
Insights
Perinatal omega-3 polyunsaturated fatty acid (PUFA) enriched diets attenuated stress-induced lactacidemia in newborn rats. Omega-3 PUFA may enhance beta-adrenergic responses and gluconeogenesis, improving outcomes in neonatal stress conditions.
Area of Science:
- Biochemistry
- Neonatal Physiology
- Nutritional Science
Background:
- Lactacidemia is a common stress response in newborns, particularly during septic shock.
- Plasma catecholamines significantly influence lactate metabolism under stress.
- Previous research indicated omega-3 polyunsaturated fatty acid (PUFA) diets attenuate endotoxic shock-induced lactacidemia in neonatal rats.
Purpose of the Study:
- To investigate the effects of perinatal omega-3 PUFA-enriched diets on catecholamine responses.
- To determine if omega-3 PUFA attenuates stress-induced lactacidemia in 10-day-old rats.
Main Methods:
- Neonatal rats were perinatally fed either omega-3 PUFA or omega-6 PUFA (control) diets.
- Lactacidemia was induced via a 5-minute swimming stress test.
- Adrenergic blockers were administered to assess catecholamine roles in swimming-induced lactacidemia.
Main Results:
- Rats fed omega-3 PUFA exhibited significantly less lactacidemia post-swimming compared to controls.
- Swimming increased plasma glucose, glucagon, hepatic cyclic adenosine monophosphate (cAMP), and phosphoenolpyruvate carboxykinase mRNA in omega-3 PUFA-fed rats.
- Adrenergic blockers differentially affected lactacidemia and hyperglycemia based on diet, suggesting altered catecholamine signaling.
Conclusions:
- Perinatal omega-3 PUFA supplementation may enhance hepatic beta-adrenergic responses and gluconeogenesis.
- These adaptations likely contribute to the observed attenuation of stress-induced lactacidemia in neonatal rats.
- Omega-3 PUFA shows potential for improving neonatal outcomes during stress and shock.
Background:
Lactacidemia is often seen under stress conditions including septic shock in the newborn. Under stress conditions, plasma catecholamine concentrations are increased and play an important role in lactate metabolism. Our previous study shows that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) attenuates lactacidemia of endotoxic shock in 10-day-old rats. In the omega-6 fatty acids series, decosapentanoic acid, two series prostaglandins and four series leukotrienes are synthesized through linoleic acids. As plasma lactate concentration correlates with the outcome of septic shock in the newborn, it is important to understand the effects of omega-3PUFA on lactate metabolism. Thus, we tested the hypothesis that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) alters responses to catecholamines and attenuates the stress-induced lactacidemia in 10-day-old rats.
Methods:
Ten-day-old rats which perinatally fed omega-3PUFA. Lactacidemia was induced by swimming for 5 min. Ten-day-old rats which perinatally fed omega-6PUFA were controls. Omega-6 fatty acids series are contained in animal fats and corn oil. Adrenergic blockers were used to assess roles of catecholamines in swimming-induced lactacidemia.
Results:
Swimming increased plasma lactate concentration less (P<0.05) in rats fed omega-3PUFA than rats fed omega-6PUFA. Swimming increased plasma concentrations of glucose and glucagon, cyclic adenosine monophosphate (cAMP) concentration and phosphoenolypruvate carboxykinase mRNA in the liver, and cAMP concentration in the hindlimb muscle more (P<0.05) in rats fed omega-3PUFA than in rats fed omega-6PUFA. Phentolamine and propranolol enhanced swim-induced lactacidemia in the omega-3PUFA group, while they decreased the lactacidemia in the omega-6PUFA group. Propranolol enhanced swimming-induced hyperglycemia in the omega-6PUFA group more than in the omega-3PUFA group.
Conclusions:
Omega-3PUFA might increase beta-adrenergic response in the liver and increase gluconeogenesis in response to stress, resulting in decreased lactacidemia.
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