What Is The Purpose Of Vitamin K – Key Laboratory of Agro-Ecological Processes in the Subtropics, Institute of Subtropical Agriculture, Chinese Academy of Sciences (CAS), China

Intestinal diseases, such as inflammatory bowel disease (IBDs) and colorectal cancer (CRC), usually characterized by clinical symptoms, malabsorption, intestinal dysfunction, injury, and microbiome imbalance, as well as some secondary intestinal disease complications, continue to be serious public health issues. Global problems. The role of vitamin K (VK) in intestinal health has attracted increasing interest in recent years. In addition to its role in blood clotting and bone health, much research continues to explore the role of VK as an emerging novel biological compound with potential action in improving gut health. This study aims to present a comprehensive review with emphasis on bacterial sources, intestinal absorption, uptake of VK, and effects of VK supplementation on immunity, anti-inflammation, intestinal microbes and its metabolites in patients with VK deficiency intestinal diseases. Promotes antioxidation, and coagulation, and epithelial development. Besides, VK-dependent proteins (VKDPs) are another important mechanism for VK to play a gastroprotection role for their anti-inflammation, immunomodulation, and anti-tumorigenesis functions. In summary, published studies preliminarily show that VK presents a beneficial effect on intestinal health and can be used as a therapeutic drug to prevent/treat intestinal diseases, but the specific mechanism of VK on intestinal health remains to be elucidated.

What Is The Purpose Of Vitamin K

Vitamin K (VK), a fat-soluble factor, is the general term for a series of structurally related compounds (1), which share a common ring structure of 2-methyl-1, 4-naphthoquinone. However, the forms of VK differ in the degree of saturation and different lengths of the aliphatic side chain attached to the 3-position (Figure 1). VK is an essential lipid-soluble vitamin that acts as a cofactor for γ-glutamyl carboxylase (GGCX), an integral membrane protein, and catalyzes the conversion of glutamate (Glu) residues to γ-carboxyglutamate (Gla) and enables VKDPs. . their biological functions (2). This biological process is inhibited by warfarin (Figure 2). In addition to the well-known biological function of blood coagulation and bone metabolism, emerging studies support VK’s involvement in many cellular and physiological processes such as oxidative stress (3, 4), immune response and anti-inflammation (5, 6), and. associated with cancer progression (7, 8) and protective and promoting roles in various organs or tissues, such as testis (9), brain (10-14), intestine (15-17), muscle (18, 19), bone (20-22 ), liver ( 7 , 23 ), kidney ( 24 , 25 ), pancreas ( 26 , 27 ), adipose tissue ( 28 – 30 ), and cardiovascular system ( 31 – 34 ) ( Fig. 3 ).

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), and (C) when n = 4 and 7, 2-methyl-3-geranyl-geranyl-1, 4-naphthoquinone (menaquinone-4, MK-4) and 2-methyl-3-all-trans-farnesyldigeranyl- 1, 4-naphthoquinone (menaquinone-7, MK-7) are two common forms of menaquinones (VK).

Figure 2 VK is required for the formation of Gla. Gla, a unique amino acid, is produced by VK-dependent post-translational modification of Glu in all Gla-containing proteins. This carboxylation process can be inhibited by warfarin.

Figure 3 Functions of VK in multi-organ systems, such as testis (9), brain (10-14), intestine (15-17), muscle (18, 19), bone (20-22), liver (7, 23). , kidney (24, 25), pancreas (26, 27), fat tissues (28-30), and cardiovascular system (31-34), and biological processes involved in anti-oxidation (3, 4), immune response. and associated with anti-inflammation (5, 6), and cancer progression (7, 8), and protective and promoting roles in various organs or tissues in the human body. The image is in a non-editable format.

The intestinal tract is the primary organ responsible for the digestion and absorption of nutrients. Also, the intestinal system fights off the invading compounds with the help of defense mechanisms such as detoxification activities and the immune system. Factors, such as nutrition, gut environment, physiological status, and microbial composition are likely to modulate gut function. Therefore, any loss in intestinal integrity can lead to enteritis, for example, in inflammatory bowel diseases (IBDs). IBDs, including both ulcerative colitis (UC) and Crohn’s disease (CD), are lifelong, chronic, immunologically inflammatory disorders of the gastrointestinal tract. This occurs as a result of altered interactions between the mucosal immune system and gut bacteria (35). The incidence of IBDs is approximately 1–3 in 1,000 individuals (36). Typical symptoms of IBDs include diarrhea, abdominal pain, and rectal bleeding (37), which are common worldwide, especially in Western countries (38). Furthermore, IBDs may increase the risk of colorectal cancer (CRC), which is the third leading cause of malignant tumors (39). An immune response to gut microbes is believed to cause IBDs in genetically susceptible individuals. The host is susceptible to colonization by pathobionts as a result of functional and structural dysbiosis of the gut microbiome. In addition, oxidative stress has a significant impact on the initiation and occurrence of relapse in UC (40). Therapeutic approaches, such as regulation of interactions between gut bacteria and the immune system, are used to restore intestinal homeostasis or reduce inflammation. In addition, when UC is in the active phase and the disease is in remission, malnutrition is responsible for approximately 85% of patients with IBD (41). Micronutrient deficiencies, such as deficiencies of VK, vitamin D, iron, selenium, zinc, folic acid, and B vitamins

Vitamin K’s Purpose For Healthy Bones & Blood Clotting

, has also been recorded in more than half of patients with IBD (41). Therefore, administration of micronutrients appears to be a novel therapeutic approach for intestinal diseases, especially those that can reduce inflammation, reduce oxidation, and prevent invasion by pathogenic bacteria. As a micronutrient, emerging evidence on the immunoregulatory effect of VK on intestinal health suggests novel roles for VK in intestinal disease health and beyond the VK specific function in hemostasis ( 13 , 32 , 42 , 43 ).

Previous studies have shown that VK reduced interleukin (IL)-6 in a murine model of colitis (44); improved antioxidant capacities (45); improved intestinal bacterial flora (15); improved intestinal alkaline phosphatase (IAP) ( 46 ), and adiponectin (ADPN), nuclear receptor vitamin D receptor (VDR), and adenosine 5′-monophosphate (AMP) activated protein kinase (AMPK) activity ( 15 ); contributing to blood coagulation in gastrointestinal bleeding (GIB) (47); and reduced IBD (16, 44) and CRC (15). Therefore, it is important to gather and summarize the latest findings on VK functions in the intestine other than aggregation and should be summarized and clarified by studies from laboratories. Current studies focus on the relationship between VK, gut health, and the mechanisms by which VK modulates gut microbes, exerts anti-inflammatory and antioxidant effects, and improves gut function.

) is present in plant margarine and vegetables ( 48 ), which are the major dietary sources of VK in the American diet ( 49 ). Vitamin K

) are a group of menaquinones (MK-n, varying from MK-4 to MK-13) found in natto, egg yolk, meat, liver, cheese, curd cheese, and butter ( 48 ) and biosynthesized by gut bacteria ( 48 ). 50). Of all the menaquinones, MK-4 and MK-7 are the best studied. Information on adequate intake of VK in detailed ingredients and natural sources was provided in a recent review (51, 52). Total VK dietary intake includes K

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, MK-4, and MK-7 (more than 60%, 24%, and 7%, respectively) (53). In animals and humans, MK-4 is catabolized from K

Intermediate to UbiA prenyltransferase domain-containing 1 (UBIAD1) ( 54 ), and partly from long-chain MKs in extrahepatic tissues, for example, salivary gland, brain, pancreas, reproductive organs, kidney, and fat ( 1 ). But when

Intake is converted to MK-4, followed by synthesis of other MKs in some but not all tissues via prenylation ( 55 ). The prenylation process appears to occur independently of intestinal bacteria (56, 57).

Apart from dietary intake sources, MKs are mainly synthesized by the gut microbiota mainly in the ileum (58). MKs are abundant in the human gut, and the concentrations of different MK forms within the gut show individual and interindividual differences associated with heterogeneity in gut microbiome composition ( 59 ). Bacteria can release MKs in lipid-soluble (60) or other forms of complexes, such as short-chain quinones (61). The major forms of MK-6 are synthesized by Eubacterium lentum, MK-7 by Veillonella, MK-8 by Escherichia coli, and MK-10 and MK-11 by Bacteroides species (50, 62). However, the disparity in faecal VK content is not due to differences in major dietary VK forms (i.e., K.

Pdf) The Extent Of Vitamin K Deficiency In Patients With Cholestatic Jaundice: A Preliminary Communication

And MK-4), but this is based on discrepancies in the molecular content of some bacterially derived MKs (63). Intestinal bacteria are capable of producing MKs, although information on the bioavailability of this intestinal MK supply is limited. Most of these MKs are bound to bacterial membranes present in the gut (1). Previous studies showed that bioactivity and bioavailability differed among vitamers (64-66), with evidence for high bioavailability, high bioactivity, and unique functions of some bacterially synthesized MK forms instead of K.

(67-69). Although gut bacteria synthesize large amounts of MKs, the bioavailability of bacterial menaquinone is generally poor, and diet is the major source of functionally available K.

(55, 70). There are studies showing that short-term reductions in dietary VK intake are not compensated by gut bacteria synthesized MKs (71, 72). In fact, inadequate dietary intake (73), restorative proctocolectomy (74), IBD (75), liver dysfunction (76). Chronic kidney disease (CKD) (77, 78), and antibiotic administration (79) can cause VK-deficient states.

Intestinal absorption of VK involves bile salt- and pancreatic-dependent solubility. Once dietary VK reaches the intestinal lumen, it is absorbed into the mix.

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