7 research outputs found
Fish oil rich diet in comparison to saturated fat rich diet offered protection against lipopolysaccharide-induced inflammation and insulin resistance in mice
<p>Abstract</p> <p>Background and Objective</p> <p>Systemic 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.</p> <p>Methods</p> <p>Twenty C57BL/6 mice were divided into two groups. One group received FO-diet and other received SF-diet <it>ad libitum </it>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.</p> <p>Results</p> <p>Food 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-1ÎČ 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.</p> <p>Conclusion</p> <p>Overall, FO-diet compared to SF-diet offered protection against deleterious effects of LPS in mice.</p
Caloric restriction favorably impacts metabolic and immune/inflammatory profiles in obese mice but curcumin/piperine consumption adds no further benefit
BACKGROUND: Obesity is associated with low-grade inflammation and impaired immune response. Caloric restriction (CR) has been shown to inhibit inflammatory response and enhance cell-mediated immune function. Curcumin, the bioactive phenolic component of turmeric spice, is proposed to have anti-obesity and anti-inflammation properties while piperine, another bioactive phenolic compound present in pepper spice, can enhance the bioavailability and efficacy of curcumin. This study sought to determine if curcumin could potentiate CRâs beneficial effect on immune and inflammatory responses in obesity developed in mice by feeding high-fat diet (HFD). METHODS: Mice were fed a HFD for 22 wk and then randomized into 5 groups: one group remained on HFD ad libitum and the remaining 4 groups were fed a 10% CR (reduced intake of HFD by 10% but maintaining the same levels of micronutrients) in the presence or absence of curcumin and/or piperine for 5 wk, after which CR was increased to 20% for an additional 33 wk. At the end of the study, mice were sacrificed, and spleen cells were isolated. Cells were stimulated with T cell mitogens, anti-CD3/CD28 antibodies, or lipopolysaccharide to determine T cell proliferation, cytokine production, and CD4(+) T cell subpopulations. RESULTS: Compared to HFD control group, all CR mice, regardless of the presence of curcumin and/or piperine, had lower body weight and fat mass, lower levels of blood glucose and insulin, and fewer total spleen cells but a higher percentage of CD4(+) T cells. Additionally, they demonstrated lower production of pro-inflammatory cytokines IL-1ÎČ and TNF-α, a trend toward lower IL-6, and lower production of PGE(2), a lipid molecule with pro-inflammatory and T cell-suppressive properties. Mice with CR alone had higher splenocyte proliferation and IL-2 production, but this effect of CR was diminished by spice supplementation. CR alone or in combination with spice supplementation had no effect on production of cytokines IL-4, IL-10, IFN-Îł, and IL-17, or the proportion of different CD4(+) T cell subsets. CONCLUSION: CR on an HFD favorably impacts both metabolic and immune/inflammatory profiles; however, the presence of curcumin and/or piperine does not amplify CRâs beneficial effects
The effect of calorie restriction with and without curcumin supplementation on inflammatory and T cellâmediated immune responses of obese mice
Continuous glucose monitoring captures glycemic variability in obesity after sleeve gastrectomy: A prospective cohort study
Abstract Objective HbA1c is an insensitive marker for assessing realâtime dysglycemia in obesity. This study investigated whether 1âh plasma glucose level (1âh PG) â„155 mg/dL (8.6 mmol/L) during an oral glucose tolerance test (OGTT) and continuous glucose monitoring (CGM) measurement of glucose variability (GV) better reflected dysglycemia than HbA1c after weight loss from metabolic and bariatric surgery. Methods This was a prospective cohort study of 10 participants with type 2 diabetes compared with 11 participants with nonâdiabetes undergoing sleeve gastrectomy (SG). At each research visit; before SG, and 6 weeks and 6 months postâSG, body weight, fasting lipid levels, and PG and insulin concentrations during an OGTT were analyzed. Mean amplitude of glycemic excursions (MAGE), a CGMâderived GV index, was analyzed. Results The 1âh PG correlated with insulin resistance markers, triglyceride/HDL ratio and triglyceride glucose index in both groups before surgery. At 6 months, SG caused 22% weight loss in both groups. Despite a reduction in HbA1c by 3.0 ± 1.3% in the diabetes group (p < 0.01), 1âh PG, and MAGE remained elevated, and the oral disposition index, which represents pancreatic ÎČâcell function, remained reduced in the diabetes group when compared to the nonâdiabetes group. Conclusions Elevation of GV markers and reduced disposition index following SGâinduced weight loss in the diabetes group underscores persistent ÎČâcell dysfunction and the potential residual risk of diabetes complications