The Small IntestineSecretions, Digestion and Motility
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
Vitamins are absorbed in different ways according to their water or fat solubility: Water-soluble vitamins: Vitamin B12 is absorbed in the terminal ileum. Intrinsic factor, which is a glycoprotein secreted by the gastric parietal cells, complexes with vitamin B12. At the ileum, the complex binds to specific receptors and becomes internalized through pinocytosis. Receptor binding requires Ca++ or Mg++ and an alkaline pH. Thiamine, vitamin C and folic acid are absorbed mainly by passive diffusion.Fat-soluble vitamins: Vitamins A, D, E and K are absorbed with other lipids and require the formation of bile salt micelles for absorption.
The patient with acute gastrointestinal problems
Ian Peate, Helen Dutton in Acute Nursing Care, 2014
Intrinsic factor binds with vitamin B12 (ingested mainly with dietary protein) to facilitate its absorption in the terminal ileum. Vitamin B12 cannot be absorbed in the absence of intrinsic factor. In pernicious anaemia, intrinsic factor is not secreted due to auto antibodies against parietal cells and B12 deficiency therefore occurs in this condition. B12 deficiency can also be due to an abnormal ileal mucosa. Because some intestinal bacteria need B12 for growth they can compete with gut cells for this substance if the normal pattern of flora is disturbed and B12 deficiency may result. ‘Blind loop syndrome’ occurs when a section of gut becomes bypassed so that digested food slows or stops moving through the intestines, leading to overgrowth of bacteria and problems in absorbing nutrients such as B12. Mucus secretion generally acts as a barrier to acid and pepsinogen which are the primary products capable of inducing injury to the mucosa.
The Role of the Clinical Laboratory in Nutritional Assessment
Aruna Bakhru in Nutrition and Integrative Medicine, 2018
Deficiencies of vitamin B12 and folate are common causes of macrocytic anemia.103 Pernicious anemia, a type of vitamin B12 anemia, is caused by insufficient production of intrinsic factor. Pernicious anemia typically occurs at 60 years of age or older.104 The etiology of vitamin B12 deficiency is diverse and includes lack of intrinsic factor, altered pH in the small intestine, and lack of absorption of B12 complexes in the terminal ileum. As with folate deficiency, poor intake of leafy vegetables can cause vitamin B12 deficiency. Other foods rich in vitamin B12 include eggs, dairy products, fortified cereal or soy beverages, tempeh, and miso (tempeh and miso are foods made from soybeans). Atrophy or loss of the gastric mucosa can prevent vitamin B12 absorption. Bacterial overgrowth in the intestine can lead to bacteria competing for cobalamin. Bowel resection and tapeworm infections, such as with Diphyllobothrium latum, also can lead to vitamin B12 deficiency.
Vitamin B12, homocysteine, and folic acid in patients suffering from bipolar disorders: Relationship with suicide
Published in The World Journal of Biological Psychiatry, 2023
Paola Mangiapane, Manuel Glauco Carbone, Alessandro Arone, Lucia Massa, Stefania Palermo, Walter Flamini, Elisabetta Parra, Benedetto Morana, Florinda Morana, Giovanni Bertini, Donatella Marazziti
Vitamin B12, also known as cobalamin, is a group-B vitamin regulating a variety of functions and requires dietary intake, as the human body cannot synthesise it (Watanabe and Bito 2018). Its sources include meat, eggs, legumes, some cheeses and others that influence its bioavailability (Allen 2010; Doets et al. 2013). Once ingested, B12 is released from animal proteins through the action of gastric factors, such as HCl and pepsin, and it is bound to a protein known as haptocorrin that is then destroyed in the intestine, thus allowing B12 to bind to a key glycoprotein, the intrinsic factor (IF) (Nielsen et al. 2012). The next step is the bonding of the B12-IF complex to the cubulin receptor in the ileum and then B12 gets transported to the plasma (Nielsen et al. 2012), where it is bound to transcobalamin and, to a greater extent, to haptocorrin, being then driven to cells or, alternatively, being stored in the liver (Carmel 2008; Stabler 2013; Miller and Green 2014).
Metformin as a potential therapeutic for neurological disease: mobilizing AMPK to repair the nervous system
Published in Expert Review of Neurotherapeutics, 2021
Sarah Demaré, Asha Kothari, Nigel A. Calcutt, Paul Fernyhough
The potential of metformin as a therapy for diabetic neuropathy has been complicated by reports of an association between long-term use of metformin and the development of vitamin B12 (cobalamin) deficiency [174]. Deficiency in B12 can lead to a form of neuropathy that is clinically indistinguishable from DSPN, characterized by symmetrical paresthesia, loss of sensation, and gait disturbances [175]. Characteristics such as age, race, time since diabetes diagnosis, and metformin dose and duration of use all likely affect the development of B12 deficiency, as well as metformin-related neuropathy [176]. However the association has been considered strong enough to prompt the American Diabetes Association to recommend periodic testing of B12 levels in those with a history of neuropathy or anemia and long-term metformin use [5]. Early research suggested that malabsorption of B12 may be the primary mechanism of deficiency, occurring in a manner independent of intrinsic factor (IF) levels [177]. Supplementation with calcium, an essential mineral for ileal B12-IF receptor function, produced partial reversal of B12 deficiency in diabetic subjects as determined by measured holotranscobalamin levels, an earlier and more sensitive measure of deficiency than serum B12, offering more support for the putative malabsorption mechanism [178]. Other mechanisms for B12 malabsorption have also been investigated [179].
Pernicious anemia: a myelodysplastic syndrome look-alike
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Yazeed Kesbeh, Zahra Pakbaz
Cytopenias and bone marrow dysplasia can be due to primary MDS or secondary to more common causes, including B12 deficiency. If a bone marrow biopsy is performed without investigating secondary causes of cytopenia, a false diagnosis of MDS may be made, causing the patient emotional trauma and unnecessary treatment with hypomethylating agents. In pernicious anemia, B12 levels can be falsely elevated in the presence of anti-intrinsic factor antibodies, therefore, checking methylmalonic acid and anti-intrinsic factor antibodies can establish the diagnosis. B12 supplementation can also affect the anti-intrinsic factor antibody assays leading to false positive results. B12 measurements should be completed before starting supplementation or delayed to at least one week after stopping B12 supplementation.