Abstract
Background and ObjectiveSystemic chronic inflammation is linked to metabolic syndrome, type-2 diabetes, and heart disease. Lipopolysaccharide (LPS), a Gram negative microbial product, triggers inflammation through toll-like-receptor-4 (TLR-4) signaling. It has been reported that dietary fatty acids also modulate inflammation through TLR-4. We investigated whether fish oil (FO) rich diet in comparison to saturated fat (SF) rich diet would confer protection from pathologies induced by LPS.MethodsTwenty C57BL/6 mice were divided into two groups. One group received FO-diet and other received SF-diet ad libitum for 60 days. Diets were isocaloric containing 45% energy from fat. After 60-days of feeding, blood was collected after overnight fast. Mice were allowed to recover for 4-days, fasted for 5-hours, challenged with 100 ng/mL of LPS intraperitonially, and bled after 2-hours. After 7-days of recuperation, mice were challenged with 500 ng/mL of LPS intraperitonially and observed for physical health.ResultsFood intake was similar in FO- and SF-fed mice. FO-fed mice compared to SF-fed mice had significantly less body weight gain (P = 0.005), epididymal fat weight (P = 0.005), fasting blood glucose (70.8 vs 83.3 ng/dL; P < 0.05), HOMA-IR (5.0 vs 13.6; P < 0.019), and serum cholesterol (167 vs 94 mg/dL; P < 0.05). When challenged with LPS, FO-fed mice had significantly lower serum IL-1β compared to SF-fed mice (2.0 vs 30.0 pg/mL; P < 0.001). After LPS-challenge, SF-fed mice had higher mortality, lost more body weight, and had greater decrease in blood glucose compared to FO-fed mice.ConclusionOverall, FO-diet compared to SF-diet offered protection against deleterious effects of LPS in mice.
Highlights
Inflammation is part of the body’s normal response to infection and injury, extreme or inappropriate inflammation is linked to the pathobiology of several diseases [1]
fish oil (FO)-fed mice compared to saturated fat (SF)-fed mice had significantly less body weight gain (P = 0.005), epididymal fat weight (P = 0.005), fasting blood glucose (70.8 vs 83.3 ng/dL; P < 0.05), Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) (5.0 vs 13.6; P < 0.019), and serum cholesterol (167 vs 94 mg/dL; P < 0.05)
After LPS-challenge, SF-fed mice had higher mortality, lost more body weight, and had greater decrease in blood glucose compared to FO-fed mice
Summary
Inflammation is part of the body’s normal response to infection and injury, extreme or inappropriate inflammation is linked to the pathobiology of several diseases [1]. Systemic low-grade chronic inflammation plays a major role in the pathogenesis of insulin resistance, metabolic syndrome, obesity, type 2 diabetes mellitus (DM2), and cardiovascular disease (CVD) [2,3,4,5]. Tolllike-receptor-4 (TLR-4) is a subclass of the TLR family involved in activation of the innate immune and inflammatory response in mammals [9,10,11] via ligation of lipopolysaccharide (LPS), a Gram-negative bacterial endotoxin found on the outer cell membrane of bacteria. Activation of TLR-4 leads to the induction of genes for many inflammatory cytokines [9,12,13,14] These cytokines are involved in inducing insulin resistance, glucose intolerance, and infiltration of macrophages into the adipose tissue which further leads to increased production of inflammatory markers [15,16,17]. We investigated whether fish oil (FO) rich diet in comparison to saturated fat (SF) rich diet would confer protection from pathologies induced by LPS
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