CD36 and DGAT2 facilitates the lipid-lowering effect of chitooligosaccharides via fatty acid intake and triglyceride synthesis signaling

2021 ◽  
Author(s):  
Xin Shen ◽  
Xinyi Liang ◽  
Xiaoguo Ji ◽  
Jiangshan You ◽  
Xinye Zhuang ◽  
...  

This study examined the impact of chitobiose (GlcN)2 and chitotriose (GlcN)3 on lipid accumulation modification and its inhibitory functionality. (GlcN)2 and (GlcN)3 was found to significantly inhibit the total cholesterol...

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Soma Roy Mitra ◽  
Pui Yee Tan ◽  
Farahnaz Amini

Gene-diet interaction studies have reported that individual variations in phenotypic traits may be due to variations in individual diet. Our study aimed to evaluate (i) the association ofADRB2rs1042713 with obesity and obesity-related metabolic parameters and (ii) the effect of dietary nutrients on these associations in Malaysian adults.ADRB2genotyping, dietary, physical activity, anthropometric, and biochemical data were collected from 79 obese and 99 nonobese individuals. Logistic regression revealed no association betweenADRB2rs1042713 and obesity (p=0.725). However, the carriers of G allele (AG + GG genotypes) of rs1042713 were associated with increased odds of insulin resistance, 2.83 (CI = 1.04–7.70, adjustedp=0.042), in the dominant model, even after adjusting for potential confounders. Obese individuals carrying the G allele were associated with higher total cholesterol (p=0.011), LDL cholesterol levels (p=0.008), and total cholesterol/HDL cholesterol ratio (p=0.048), compared to the noncarriers (AA), even after adjusting for potential confounders. Irrespective of obesity, the carriers of GG genotype had significantly lower fasting glucose levels with low saturated fatty acid intake (<7.3% of TE/day) (4.92 ± 0.1 mmol/L vs 5.80 ± 0.3 mmol/L,p=0.011) and high intake of polyunsaturated fatty acid:saturated fatty acid ratio (≥0.8/day) (4.83 ± 0.1 mmol/L vs 5.93 ± 0.4 mmol/L,p=0.006). Moreover, the carriers of GG genotype with high polyunsaturated fatty acid intake (≥6% of TE/day) had significantly lower HOMA-IR (1.5 ± 0.3 vs 3.0 ± 0.7,p=0.026) and fasting insulin levels (6.8 ± 1.6 µU/mL vs 11.4 ± 2.1 µU/mL,p=0.036). These effects were not found in the noncarriers (AA). In conclusion, G allele carriers ofADRB2rs1042713 were associated with increased odds of insulin resistance. Obese individuals carrying G allele were compromised with higher blood lipid levels. Although it is premature to report gene-diet interaction on the regulation of glucose and insulin levels in Malaysians, we suggest that higher quantity of PUFA-rich food sources in regular diet may benefit overweight and obese Malaysian adults metabolically. Large-scale studies are required to replicate and confirm the current findings in the Malaysian population.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Hui-Kang Liu ◽  
Tzu-Min Hung ◽  
Hsiu-Chen Huang ◽  
I-Jung Lee ◽  
Chia-Chuan Chang ◽  
...  

Obesity and associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are currently a worldwide health problem. In Asian traditional medicine, Bai-Hu-Jia-Ren-Shen-Tang (BHJRST) is widely used in diabetes patients to reduce thirst. However, whether it has a therapeutic effect on T2DM or NAFLD is not known. The aim of this study was to examine whether BHJRST had a lipid-lowering effect using a HuS-E/2 cell model of fatty liver induced by palmitate and in a db/db mouse model of dyslipidemia. Incubation of HuS-E/2 cells with palmitate markedly increased lipid accumulation and expression of adipose triglyceride lipase (ATGL), which is involved in lipolysis. BHJRST significantly decreased lipid accumulation and increased ATGL levels and phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream target, acetyl-CoA carboxylase (ACC), which are involved in fatty acid oxidation. Furthermore, after twice daily oral administration for six weeks, BHJRST significantly reduced hepatic fat accumulation in db/db mice, as demonstrated by increased hepatic AMPK and ACC phosphorylation, reduced serum triglyceride levels, and reduced hepatic total lipid content. The results show that BHJRST has a lipid-lowering effect in the liver that is mediated by activation of the AMPK signaling pathway.


1997 ◽  
Vol 13 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Augustine S Aruna ◽  
Shiva K Akula ◽  
Daniel F Sarpong

Objective: To evaluate the potential impact of potassium-depleting diuretics on the efficacy of lovastatin. Design: A retrospective study of ambulatory patients taking lovastatin and thiazide or loop diuretics was conducted. Setting: Ambulatory care patients with coexisting hypercholesterolemia and hypertension from a Veterans Affairs Medical Center. Participants: A total of 32 patients were studied, 13 of whom had been taking lovastatin before diuretics were added. Another 19 patients had been receiving diuretics before lovastatin was initiated. The changes in their total cholesterol from baseline were recorded and analyzed. Main Outcome Measures: In all the patients taking lovastatin and diuretics concurrently, total cholesterol concentrations dropped initially, followed by a rise despite continuation of therapy with lovastatin. The reason for this initial drop in total cholesterol following 1 month of concurrent therapy is the subject of further investigation in a prospective study. Results: Regardless of the order of administration of the lipid-lowering and antihypertensive drugs, serum cholesterol rose 20% from its nadir. Conclusions: Patients taking potassium-depleting diuretics and a hepatic hydroxymethylglutaryl-coenzyme A reductase enzyme inhibitor (lovastatin) concurrently do not seem to benefit substantially from the lipid-lowering effect of lovastatin, probably because of a functional antagonism of the lipid-lowering effect of lovastatin by potassium-depleting diuretics.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Maryam Zaid ◽  
Katsuyuki Miura ◽  
Akira Fujiyoshi ◽  
Akira Okayama ◽  
Hideaki Nakagawa ◽  
...  

Background: Studies have found that HDL particle (HDL-P) concentration is inversely associated with risk of CVD, independent of HDL cholesterol (HDL-C). Dietary factors (such as fatty acid intake) have been found to affect levels of HDL-C and influence risk of CVD. However, little is known about the associations of dietary fatty acid with serum HDL-P levels. Hypothesis: We hypothesized that dietary fatty acid associations with HDL-P are independent of HDL-C in men. Methods: Data were from 463 male participants in the 1996-98 cross-sectional INTERLIPID Study, ages 40-59 years, randomly selected from five populations; four in Japan (n=386) and one in Hawaii (n=77). Fatty acid intake was estimated from the mean of four in-depth 24-hour dietary recalls (% kcal per day). Individuals were excluded due to missing data on HDL-P or HDL-C and use of lipid lowering medication. Serum HDL-P was measured using nuclear magnetic resonance and HDL-C was measured using standard methods. Multiple linear regression models were used to assess the association between dietary fatty acid and each of the lipid measures. Results: In men, HDL-P and HDL-C were moderately correlated (r = 0.52, p<0.001). In Model 1 (Table), adjusted for age, country, alcohol intake, BMI, diabetes, hypertension, smoking status, and physical activity, most dietary fatty acids were significantly (p<0.05) associated with HDL-P and HDL-C levels. In Model 2, further adjusted for HDL-C, almost all fatty acids maintained a significant association with HDL-P. In contrast, most associations of fatty acids and HDL-C ceased to be significant after adjustment for HDL-P. Total SFA and omega-3 PUFA remained associated with HDL-C. Conclusion: HDL-P was significantly associated with fatty acid intake, independent of HDL-C. Associations of dietary fatty acid intake and HDL-C level were weaker and generally not independent of HDL-P in men.


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