Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Jan 4;11(1):86.
doi: 10.3390/nu11010086.

Effect of Wakame and Carob Pod Snacks on Non-Alcoholic Fatty Liver Disease

Affiliations

Effect of Wakame and Carob Pod Snacks on Non-Alcoholic Fatty Liver Disease

Daniel Rico et al. Nutrients. .

Abstract

Snacks combining different functional ingredients could represent a useful therapeutic strategy against NAFLD. The present study aimed to analyze the effect of two snack formulations based on carob and wakame flour in the treatment for NAFLD in rats. For this purpose, metabolic syndrome was induced in 50 adult rats by a high-fat high-fructose diet over eight weeks. After this period, rats were fed either normal calorie diets supplemented or not with snack A (1/50 wakame/carob pod) and snack B (1/5 wakame/carob pod) for four additional weeks. After sacrifice, liver composition and serum parameters were analyzed. Different pathways of triacylglycerol metabolism in liver were studied including fatty acid oxidation, fatty acid synthesis, triglyceride assembly and release, fatty acid uptake and glucose uptake. Oxidative stress was also measured. Snack treatment, and mainly B snack, reduced liver triacylglycerol levels by increasing fat oxidation. Moreover, this snack reduced oxidative stress. Therefore, this snack formulation could represent an interesting tool useful for fatty liver treatment.

Keywords: NAFLD; carob; snack; steatohepatitis; wakame.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Effects on oxidative stress of MetS rats (MS), rats with fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) TBARS activity and (B) SOD activity. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05).
Figure 2
Figure 2
Effects on fatty acid oxidation of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Oxidative genes mRNA levels, (B) CPT activity, and (C) CS activity. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05). In the case of CPT1a and CS activities, p value for the comparisons SM and SB groups or OC and SB groups is p < 0.001.
Figure 3
Figure 3
Effects on fatty acid synthesis of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Fatty acid synthesis involved genes mRNA levels, (B) FAS activity and (C) PK activity. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05). In the case of cherb gene expression, p value for the comparison between MS, OC and SA is p < 0.01.
Figure 4
Figure 4
Effects on triacylglycerol re-esterification and triacylglycerol release of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) triacylglycerol re-esterification involved genes mRNA levels and (B) MTP activity. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05).
Figure 4
Figure 4
Effects on triacylglycerol re-esterification and triacylglycerol release of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) triacylglycerol re-esterification involved genes mRNA levels and (B) MTP activity. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05).
Figure 5
Figure 5
Effects on fatty acid uptake of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Fatty acid uptake involved genes mRNA levels, (B) FATP2 protein levels and (C) FATP5 protein levels. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05). In the case of acsl1 gene expression, p value for the comparison between OC and SA vs. SB is p < 0.01.
Figure 5
Figure 5
Effects on fatty acid uptake of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Fatty acid uptake involved genes mRNA levels, (B) FATP2 protein levels and (C) FATP5 protein levels. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05). In the case of acsl1 gene expression, p value for the comparison between OC and SA vs. SB is p < 0.01.
Figure 6
Figure 6
Effects on glucose uptake of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Glucose uptake involved genes mRNA levels, (B) GLUT2 protein levels and (C) GLUT5 protein levels. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05).
Figure 6
Figure 6
Effects on glucose uptake of MetS rats (MS, n = 10), rats fed with wheat control diet (WC, n = 10), wheat and oat control diet (OC, n = 10), A snack (SA, n = 10), and B snack (SB, n = 10). (A) Glucose uptake involved genes mRNA levels, (B) GLUT2 protein levels and (C) GLUT5 protein levels. Values are expressed as mean ± SEM. Values not sharing a common letter are significantly different (p < 0.05).

Similar articles

Cited by

References

    1. Schwenger K.J.P., Bolzon C.M., Li C., Allard J.P. Non-alcoholic fatty liver disease and obesity: The role of the gut bacteria. Eur. J. Nutr. 2018 doi: 10.1007/s00394-018-1844-5. - DOI - PubMed
    1. Vernon G., Baranova A., Younossi Z.M. Systematic review: The epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults. Aliment Pharmacol. Ther. 2011;34:274–285. doi: 10.1111/j.1365-2036.2011.04724.x. - DOI - PubMed
    1. Sayiner M., Koenig A., Henry L., Younossi Z.M. Epidemiology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis in the United States and the Rest of the World. Clin. Liver Dis. 2016;20:205–214. doi: 10.1016/j.cld.2015.10.001. - DOI - PubMed
    1. Softic S., Cohen D.E., Kahn C.R. Role of Dietary Fructose and Hepatic De Novo Lipogenesis in Fatty Liver Disease. Dig. Dis. Sci. 2016;61:1282–1293. doi: 10.1007/s10620-016-4054-0. - DOI - PMC - PubMed
    1. Airanthi M.K., Sasaki N., Iwasaki S., Baba N., Abe M., Hosokawa M., Miyashita K. Effect of brown seaweed lipids on fatty acid composition and lipid hydroperoxide levels of mouse liver. J. Agric. Food Chem. 2011;59:4156–4163. doi: 10.1021/jf104643b. - DOI - PubMed

MeSH terms