The substances produced by the gut microbiome are known as postbiotics, and, according to the latest research, postbiotic compounds appear to be highly beneficial and essential for optimal health.

To understand postbiotics, we need to understand both probiotics and prebiotics. Probiotics are “live microorganisms which, when administered in adequate amounts, confer a health benefit on the host.” These probiotics, or “good bacteria,” digest the prebiotic compounds in the gut, which include dietary fiber and other substances naturally found in food, to produce the postbiotics.^1,2 A postbiotic can be defined as a “preparation of inanimate microorganisms and/or their components that confers a health benefit on the host.” So, postbiotic preparations can contain inactivated probiotic bacteria and/or the compounds secreted by these bacteria.³

Postbiotic substances produced by probiotic bacteria include enzymes, bioactive peptides, short-chain fatty acids, antimicrobial peptides, polysaccharides, cell surface proteins, vitamins, plasmalogens, organic acids, and other healthy compounds. Since the production of beneficial postbiotic compounds is not guaranteed, even with probiotic and prebiotic supplementation, researchers are now producing postbiotics in controlled environments outside the gut to assess their beneficial effects in studies. Postbiotic compounds are now also available as dietary supplements.

The Liver

The liver is a football-sized organ located on the right side of the body, just underneath the rib cage, and it is responsible for numerous processes in the body.

Some critical functions of the liver include:

• Nutrient metabolism and storage⁴
• Blood volume regulation⁴
• Blood sugar production, storage, and release⁴
• Immune system support⁴
• Endocrine control of growth signaling pathways⁴
• Lipid and cholesterol homeostasis⁴
• Production and secretion of blood proteins⁴
• Processing of amino acids for energy and disposal of the waste products from the breakdown of proteins⁴
• Detoxification of xenobiotics and other substances⁵

Insulin Resistance

One health concern becoming more prevalent is insulin resistance. Insulin resistance is closely associated with several other health conditions, including type II diabetes, nonalcoholic fatty liver disease (NAFLD), obesity, and cardiovascular disease.⁴ Insulin is a hormone secreted by the pancreas. Insulin regulates blood sugar levels by binding to insulin receptors on cell membranes. While all cells have insulin receptors, the cells with the highest density of insulin receptors are liver cells and fat cells. When the insulin hormone attaches to its receptor on a cell, it allows sugar to move from the blood into the cell, thus reducing the blood sugar level.⁶ In a balanced system, the sugar shuttled into the cells will be used. When too much sugar or insulin is present; though, the sugar is often transformed into fat for storage purposes. Insulin drives fat storage, and the presence of an excessive amount of insulin is an underlying cause of obesity.⁷

In general, insulin resistance occurs when the tissues are no longer able to respond adequately to normal insulin levels. When sugar is not shuttled into cells efficiently, the blood sugar level rises, which then stimulates the pancreas to release more insulin, leading to higher blood insulin levels.^8,9 The elevated insulin level then sets the stage for many modern diseases, including metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), atherosclerosis, and type II diabetes, as the insulin and blood glucose levels increase over time.⁸

As mentioned above, critical liver functions include the production, storage, and release of sugar to optimize the blood sugar level.⁴ The presence of insulin decreases blood sugar production in the liver because, when insulin is present, blood sugar is being cleared from the blood, so the liver does not need to produce more sugar. But, when insulin resistance is present in the liver, the insulin no longer decreases sugar production, which then further increases the blood sugar level. While the inhibitory effect of insulin on blood sugar release is lost due to insulin resistance, the stimulatory effect of insulin on fat production is maintained in the liver. This complex phenomenon is known as ‘selective insulin resistance,’ which contributes to the harmful consequences of insulin resistance, especially nonalcoholic fatty liver disease (NAFLD).⁴

What is nonalcoholic fatty liver disease (NAFLD)?

NAFLD is a liver disorder that is closely associated with insulin resistance and far more common than hepatitis. NAFLD affects nearly 25% of people in the world and up to 30% of individuals in Western countries; therefore, approximately one out of every four people you know probably has NAFLD.^10,11 NAFLD is diagnosed via imaging and sometimes an invasive liver biopsy, so while NAFLD is rampant, many who have NAFLD are unaware. The number of individuals with NAFLD continues to increase at an alarming pace as metabolic disorders including obesity, Type 2 Diabetes, and insulin resistance also increase worldwide. The most severe cases of NAFLD lead to the development of cirrhosis of the liver, and NAFLD is expected to become the leading cause of liver transplantation due to cirrhosis in the near future.¹⁰

NAFLD is characterized by increased fat accumulation in the liver in the absence of excessive alcohol consumption.¹¹ Excessive alcohol consumption also causes a fatty liver to develop, but the increase in fat accumulation in the liver in NAFLD is related to metabolic dysfunction, which often includes insulin resistance, elevated cholesterol levels, obesity, and high blood pressure.¹¹ The severity of NAFLD varies significantly and ranges from simple fatty liver to an inflammatory condition known as non-alcoholic steatohepatitis (NASH), which may advance to cirrhosis and liver cancer.^11,12

While insulin resistance is known to induce NAFLD, substances secreted from fat tissue called adipokines could also contribute to its development. Ongoing research continues to bring attention to the roles the gut microbiome and the gut-liver axis play in the pathogenesis and progression of NAFLD and the most common causes of NAFLD, including insulin resistance.^11,13

Adiponectin

Adiponectin is one adipokine that appears to protect the liver from NAFLD. According to research, one of the mechanisms by which adiponectin can prevent NAFLD is by promoting the use of fat as energy, which then prevents the excessive production and storage of fat, improves insulin sensitivity, and reduces the risk of cardiovascular disease.¹¹ In fact, research shows the higher the adiponectin level, the lower the liver fat content.¹⁴ Therefore, interventions that increase adiponectin might offer a golden ticket to ameliorate NAFLD and NAFLD-related complications.^11,14

Do postbiotics support liver health?

According to the latest research, the answer is YES!

An animal study that assessed the effects of a diet high in supplemental pectin, a prebiotic, concluded the high-pectin diet increased circulating levels of the bioactive postbiotic compound acetate. The postbiotic acetate then facilitated the significantly increased production of key adipokines, especially adiponectin, to prevent obesity and modulate fat metabolism and storage in the liver.¹⁵ Another animal study by Lu et al. confirmed the presence of increased mRNA levels of the adipokines adiponectin and resistin in mice who consumed a diet supplemented with either dietary acetate, propionate, butyrate, or a mixture of all three postbiotic compounds. The researchers concluded postbiotics are likely helpful for the prevention of insulin resistance and obesity. The researchers noted evidence that short-term consumption of these postbiotic compounds can alleviate diet-induced obesity and insulin resistance through several mechanisms. The mechanisms include activation of the adiponectin-mediated pathway, stimulation of mitochondrial function in muscles, and the regulation of whole-body insulin sensitivity by the adipokine resistin. The higher the resistin level, the lower the risk of developing insulin resistance.¹⁶

Additional animal studies confirm supplemental inulin, another prebiotic, also positively alters the gut microbiome by increasing the production of postbiotics, which results in powerful protection against diet-induced obesity, a reduction of fat accumulation in the liver, and a decrease in blood sugar levels.¹⁷ A very recent and unique animal study looked at the effect of a postbiotic preparation that included heat-killed probiotics. The administration of heat-killed Lactiplantibacillus plantarum LRCC5314 did significantly increase the expression of adiponectin, which is consistent with the effect of postbiotics in the other animal studies.¹⁸ While most of the research consists of preclinical animal studies, at least one clinical trial in humans confirms the postbiotic compound propionate prevents fat accumulation in the liver.¹⁹

There is an impressive amount of high-quality preclinical research that strongly suggests a significant link between the gut microbiome and liver diseases such as NAFLD. Therefore, it is logical to develop new treatment strategies that support the gut–liver axis. Postbiotics, the nourishing substances produced by the gut microbiome, are a highly promising therapeutic option.

Postbiotic compounds are available in our NEW IPX-Booster and IPX-Booster Super Strength supplements!*

SUPPLEMENTation WITH IPX-Booster Super Strength

• Supports the structural integrity of the GI tract*
• Maintains a healthy gut microbiome*
• Enhances adiponectin production to support healthy liver function*
• Supports healthy insulin, glucose, and cholesterol levels*
• Provides anti-inflammatory benefits*
• Stimulates the production of protective sIgA antibodies*
• Balances immune system function*
• Supports healthy blood pressure levels*
• Promotes optimal cellular health and functionality*
• Promotes healthy cortisol levels*

* This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.

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References:

1. Knackstedt R, Knackstedt T, Gatherwright J. The role of topical probiotics in skin conditions: A systematic review of animal and human studies and implications for future therapies. Exp Dermatol. 2020;29(1):15-21. doi:10.1111/exd.14032

2. Gibson GR, Hutkins R, Sanders ME, et al. Expert consensus document: The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of prebiotics. Nat Rev Gastroenterol Hepatol. 2017;14(8):491-502. doi:10.1038/nrgastro.2017.75

3. Salminen S, Collado MC, Endo A, et al. The International Scientific Association of Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of postbiotics [published correction appears in Nat Rev Gastroenterol Hepatol. 2021 Jun 15;:]. Nat Rev Gastroenterol Hepatol. 2021;18(9):649-667. doi:10.1038/s41575-021-00440-6

4. Trefts E, Gannon M, Wasserman DH. The liver. Curr Biol. 2017;27(21):R1147-R1151. doi:10.1016/j.cub.2017.09.019

5. Aronica L, Ordovas JM, Volkov A, et al. Genetic Biomarkers of Metabolic Detoxification for Personalized Lifestyle Medicine. Nutrients. 2022;14(4):768. doi:10.3390/nu14040768

6. Thota S, Akbar A. Insulin - StatPearls - NCBI Bookshelf - ncbi.nlm.nih.gov. https://www.ncbi.nlm.nih.gov/books/NBK560688/. Published July 16, 2021. Accessed May 18, 2022.

7. Kolb H, Kempf K, Röhling M, Martin S. Insulin: too much of a good thing is bad. BMC Med. 2020;18(1):224. doi:10.1186/s12916-020-01688-6

8. Lee SH, Park SY, Choi CS. Insulin Resistance: From Mechanisms to Therapeutic Strategies. Diabetes Metab J. 2022;46(1):15-37. doi:10.4093/dmj.2021.0280

9. Tokarz VL, MacDonald PE, Klip A. The cell biology of systemic insulin function. J Cell Biol. 2018;217(7):2273-2289. doi:10.1083/jcb.201802095

10. Maurice J, Manousou P. Non-alcoholic fatty liver disease. Clin Med (Lond). 2018;18(3):245-250. doi:10.7861/clinmedicine.18-3-245

11. Shabalala SC, Dludla PV, Mabasa L, et al. The effect of adiponectin in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and the potential role of polyphenols in the modulation of adiponectin signaling. Biomed Pharmacother. 2020;131:110785. doi:10.1016/j.biopha.2020.110785

12. Johnston MP, Patel J, Byrne CD. Causes of Mortality in Non-Alcoholic Fatty Liver Disease (NAFLD) and Alcohol Related Fatty Liver Disease (AFLD). Curr Pharm Des. 2020;26(10):1079-1092. doi:10.2174/1381612826666200128094231

13. Wang W, Xu AL, Li ZC, et al. Combination of Probiotics and Salvia miltiorrhiza Polysaccharide Alleviates Hepatic Steatosis via Gut Microbiota Modulation and Insulin Resistance Improvement in High Fat-Induced NAFLD Mice. Diabetes Metab J. 2020;44(2):336-348. doi:10.4093/dmj.2019.0042

14. Achari AE, Jain SK. Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction. Int J Mol Sci. 2017;18(6):1321. doi:10.3390/ijms18061321

15. García-Carrizo F, Cannon B, Nedergaard J, et al. Regulation of thermogenic capacity in brown and white adipocytes by the prebiotic high-esterified pectin and its postbiotic acetate. Int J Obes (Lond). 2020;44(3):715-726. doi:10.1038/s41366-019-0445-6

16. Lu Y, Fan C, Liang A, et al. Effects of SCFA on the DNA methylation pattern of adiponectin and resistin in high-fat-diet-induced obese male mice. Br J Nutr. 2018;120(4):385-392. doi:10.1017/S0007114518001526

17. Igarashi M, Morimoto M, Suto A, et al. Synthetic dietary inulin, Fuji FF, delays development of diet-induced obesity by improving gut microbiota profiles and increasing short-chain fatty acid production. PeerJ. 2020;8:e8893. doi:10.7717/peerj.8893

18. Nam Y, Yoon S, Baek J, et al. Heat-Killed Lactiplantibacillus plantarum LRCC5314 Mitigates the Effects of Stress-Related Type 2 Diabetes in Mice via Gut Microbiome Modulation. J Microbiol Biotechnol. 2022;32(3):324-332. doi:10.4014/jmb.2111.11008

19. Chambers ES, Preston T, Frost G, et al. Role of Gut Microbiota-Generated Short-Chain Fatty Acids in Metabolic and Cardiovascular Health. Curr Nutr Rep. 2018;7(4):198-206. doi:10.1007/s13668-018-0248-8