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
Review
. 2018 Jul 21;10(7):943.
doi: 10.3390/nu10070943.

Dietary Fibre as a Unifying Remedy for the Whole Spectrum of Obesity-Associated Cardiovascular Risk

Affiliations
Review

Dietary Fibre as a Unifying Remedy for the Whole Spectrum of Obesity-Associated Cardiovascular Risk

Lutgarda Bozzetto et al. Nutrients. .

Abstract

Obesity is a pandemic carrying the heavy burden of multiple and serious co-morbidities including metabolic syndrome, type 2 diabetes and cardiovascular diseases. The pathophysiological processes leading to the accumulation of body fat slowly evolve to fat accumulation in other body compartments than subcutaneous tissue. This abnormal fat deposition determines insulin resistance which in turn causes blood glucose and lipid metabolism derangement, non-alcoholic fatty liver disease, hypertension, and metabolic syndrome. All these conditions contribute to increase the cardiovascular risk of obese people. Several randomized clinical trials demonstrated that moderate weight loss (5⁻10%) in obese patients improves obesity-related metabolic risk factors and coexisting disorders. Therefore, nutritional strategies able to facilitate weight management, and in the meantime positively influence obesity-associated cardiovascular risk factors, should be implemented. To this aim, a suitable option could be dietary fibres that may also act independently of weight loss. The present narrative review summarizes the current evidence about the effects of dietary fibres on weight management in obese people. Moreover, all of the different cardiovascular risk factors are individually considered and evidence on cardiovascular outcomes is summarized. We also describe the plausible mechanisms by which different dietary fibres could modulate cardio-metabolic risk factors. Overall, despite both epidemiological and intervention studies on weight loss that show statistically significant but negligible clinical effects, dietary fibres seem to have a beneficial impact on main pathophysiological pathways involved in cardiovascular risk (i.e., insulin resistance, renin-angiotensin, and sympathetic nervous systems). Although the evidence is not conclusive, this suggests that fibre would be a suitable option to counteract obesity-related cardio-metabolic diseases also independently of weight loss. However, evidence is not consistent for the different risk factors, with clear beneficial effects shown on blood glucose metabolism and Low Density Lipoprotein (LDL) cholesterol while there is fewer, and less consistent data shown on plasma triglyceride and blood pressure. Ascribing the beneficial effect of some foods (i.e., fruits and vegetables) solely to their fibre content requires more investigation on the pathophysiological role of other dietary components, such as polyphenols.

Keywords: cardiovascular risk; diabetes type 2; dietary fibre; dyslipidemia; hypertension; insulin resistance; metabolic syndrome; obesity.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathophysiological mechanisms by which excessive adipose tissue leads to metabolic dysfunction and common chronic diseases. RAS: renin-angiotensin system; SNS: sympathetic nervous system; FFA: free fatty acids; IL-6: interleukin-6; IL-1β: interleukin-1β; TNF-α: tumor necrosis factor-α.
Figure 2
Figure 2
Plausible mechanisms of action whereby fibre may influence body weight and its related common chronic diseases.CCK: cholecystokinin; GIP: gastric inhibitory peptide; GLP-1: glucagon like peptide 1; SCFA: short chain fatty acids.

References

    1. The GBD 2015 Obesity Collaborators Health Effects of Overweight and Obesity in 195 Countries over 25 Years. N. Engl. J. Med. 2017;377:13–27. - PMC - PubMed
    1. Pigeyre M., Yazdi F.T., Kaur Y., Meyre D. Recent progress in genetics, epigenetics and metagenomics unveils the pathophysiology of human obesity. Clin. Sci. 2016;130:943–986. doi: 10.1042/CS20160136. - DOI - PubMed
    1. Van der Klaauw A.A., Farooqi I.S. The hunger genes: Pathways to obesity. Cell. 2015;161:119–132. doi: 10.1016/j.cell.2015.03.008. - DOI - PubMed
    1. Grant R.W., Dixit V.D. Adipose tissue as an immunological organ. Obesity. 2015;23:512–518. doi: 10.1002/oby.21003. - DOI - PMC - PubMed
    1. Bozzetto L., Prinster A., Mancini M., Giacco R., De Natale C., Salvatore M., Riccardi G., Rivellese A.A., Annuzzi G. Liver fat in obesity: Role of type 2 diabetes mellitus and adipose tissue distribution. Eur. J. Clin. Investig. 2011;41:39–44. doi: 10.1111/j.1365-2362.2010.02372.x. - DOI - PubMed

MeSH terms

LinkOut - more resources