"Retinol-induced Intestinal Tumorigenesis in Min/+ Mice and Importance of Vitamin D Status.
Hetland RB, Alexander J, Berg JP, Svendsen C, Paulsen JE.
Anticancer Res. 2009 Nov;29(11):4353-60.
PMID: 20032378
The effects of life-long dietary exposure, starting in utero, to high retinol, low vitamin D, or high retinol in combination with low vitamin D on Intestinal tumorigenesis in Min/+ mice were investigated. In males, high retinol alone significantly increased the number (2.6-fold) and size (1.3-fold) of small Intestinal tumours; in females no significant increase in tumour number or size was seen. In both genders, low vitamin D intake alone did not affect Intestinal tumorigenesis. In males, intake of the combined high retinol/low vitamin D diet did not further increase the effects caused by high retinol alone. In females, however, the high retinol/low vitamin D-induced increase in tumour number (3.1-fold) and tumour size (1.5-fold) exceeded that of high retinol alone. In conclusion, a high dietary intake of retinol stimulated Intestinal tumorigenesis in Min/+ mice. Furthermore, the results indicate a combined effect of high retinol and low vitamin D on tumorigenesis in females"
"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University.
They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol.
They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."
Acid-base balance has an effect on bone turnover, especially on the rates of bone resorption and calcium mobilization. Bone mineral participates in the defense against acid-base disturbances, especially against metabolic acidosis (Lemann et al. 1966, Green & Kleeman 1991). The role of the bone mineral is important in the acid-base disorders, as no appreciable change in the intestinal calcium absorption occurs (Bichara et al. 1990).
In the mammalian body, mainly three hormones regulate the calcium metabolism and the bone turnover. 1,25-dihydroxycholecalciferol (vitamin D derivative) increases calcium absorption from the intestine and, indirectly, from bone. Parathyroid hormone mobilizes calcium from the bone and increases the urinary phosphate excretion. Calcitonin inhibits bone resorption (Ganong 1981). Used as drugs, these hormones are also capable of inducing acid-base disorders. Calcitonin administration (Escanero et al. 1991) and vitamin D excess (Bichara et al. 1990) have been reported to cause metabolic alkalosis.
Coconut kernel protein modifies the effect of coconut oil on serum lipids.
Padmakumaran Nair KG, Rajamohan T, Kurup PA.
Plant Foods Hum Nutr. 1999;53(2):133-44.
PMID: 10472790
DOI: 10.1023/A:1008078103299
Feeding coconut kernel along with coconut oil in human volunteers has been found to reduce serum total and LDL cholesterol when compared to feeding coconut oil alone. This effect of the kernel was also observed in rats. Since many plant proteins have been reported to exert a cholesterol lowering effect, a study was carried out on the effect of isolated kernel protein in rats. Feeding kernel protein resulted in lower levels of cholesterol, phospholipids and triglycerides in the serum and most tissues when compared to casein fed animals. Rats fed kernel protein had (1) increased hepatic degradation of cholesterol to bile acids, (2) increased hepatic cholesterol biosynthesis, and (3) decreased esterification of free cholesterol. In the intestine, however, cholesterogenesis was decreased. The kernel protein also caused decreased lipogenesis in the liver and intestine. This beneficial effect of the kernel protein is attributed to its very low lysine/arginine ratio 2.13% lysine and 24.5% arginine....
[Vitamin K and Bone Update. In vivo Metabolism of Vitamin K. - In relation to the conversion of vitamin K(1) to MK-4 -]
Okano T, Nakagawa K, Kamao M.
Clin Calcium. 2009 Dec;19(12):1779-87. Japanese.
PMID: 19949269
Phylloquinone is a major form (>90%) of dietary vitamin K, but the form of vitamin K that exists at the highest concentrations in tissues of animals and humans is menaquinone-4 (MK-4) . Despite this great difference, the origin of tissue MK-4 had not been clarified until recently. We demonstrated that deuterium-labeled phylloquinone was converted into deuterium-labeled MK-4 in mice and this conversion occurred following an oral or enteral administration, but not parenteral administration. By the oral route, the phylloquinone with the deuterium-labeled side chain (phytyl side-chain) was clearly converted into menaquinone-4 with a non-deuterium-labeled side chain (geranylgeranyl side-chain) , implying that phylloquinone was converted into menaquinone-4 via integral side-chain removal. Our results suggest that cerebral menaquinone-4 originates from phylloquinone intake and the release of menadione from phylloquinone in the intestine followed by the prenylation of menadione into menaquinone-4 in the intestine or tissues
The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets.
Thacher TD, Obadofin MO, O'Brien KO, Abrams SA.
J Clin Endocrinol Metab. 2009 Sep;94(9):3314-21. Epub 2009 Jun 30.
PMID: 19567516
Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption
It is an inflammatory, refractory disease which includes colon, rectum and little part of small intestine. The person who is suffering from Ulcerative colitis in tests shows ulcers inside the colon. Ulcerative colitis comes under the category of ...
It is an inflammatory, refractory disease which includes colon, rectum and little part of small intestine. The person who is suffering from Ulcerative colitis in tests shows ulcers inside the colon. Ulcerative colitis comes under the category of ...
Vitamin D A Key Player In Overall Health Of Several Body Organs, Says Biochemist
In a paper published in the August issue of the American Journal of Clinical Nutrition, Norman identifies vitamin D's potential for contributions to good health in the adaptive and innate immune systems, the secretion and regulation of insulin by the pancreas, the heart and blood pressure regulation, muscle strength and brain activity. In addition, access to adequate amounts of vitamin D is believed to be beneficial towards reducing the risk of cancer.
Norman also lists 36 organ tissues in the body whose cells respond biologically to vitamin D. The list includes bone marrow, breast, colon, intestine, kidney, lung, prostate, retina, skin, stomach and the uterus.
Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier.
Kong J, Zhang Z, Musch MW, Ning G, Sun J, Hart J, Bissonnette M, Li YC.
Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G208-16. Epub 2007 Oct 25.
PMID: 17962355
These observations suggest that VDR plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium. Therefore, vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD.
Synbiotic effect of Lactobacillus helveticus M92 and prebiotics on the intestinal microflora and immune system of mice.
Frece J, Kos B, Svetec IK, Zgaga Z, Beganović J, Lebos A, Susković J.
J Dairy Res. 2009 Feb;76(1):98-104. Epub 2009 Jan 5.
PMID: 19121230
doi:10.1017/S0022029908003737
"Results indicated that mice on diets supplemented with flaxseed meal and flaxseed oil had, on average, 45 percent fewer tumors in the small intestine and the colon compared to the control group."
The scientists published their research findings in February in the academic peer-reviewed international journal Nutrition and Cancer.
Natural Sphingadienes Inhibit Akt-Dependent Signaling and Prevent Intestinal Tumorigenesis.
Fyrst H, Oskouian B, Bandhuvula P, Gong Y, Byun HS, Bittman R, Lee AR, Saba JD.
Cancer Res. 2009 Nov 24. [Epub ahead of print]
PMID: 19934323
DOI: 10.1158/0008-5472.CAN-09-2341
What is diverticulitis and what signs and symptoms occur when you have diverticulitis? What Foods You Should Eat If You Have Diverticulitis and what you should not eat when you discovered you have diverticulitis. Described many causes in this article if you are looking for causes of diverticulitis.
Diverticulitis is a very serious medical condition. It causes inflamed pouches in the lining of your intestine. It is a very serious medical condition that causes infection or inflammation of small pouches in the lining of your intestine that is known as diverticula that develop along the walls of the intestines.
Although it is not a condition that is commonly accepted by most medical practitioners, leaky gut syndrome is nonetheless a disease from which many people claim to suffer. Leaky gut syndrome is purportedly a condition that affects the intestinal lining whereby unwanted substances such as toxins "leak" into the bloodstream.
Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density.
Abreu MT, Kantorovich V, Vasiliauskas EA, Gruntmanis U, Matuk R, Daigle K, Chen S, Zehnder D, Lin YC, Yang H, Hewison M, Adams JS.
Gut. 2004 Aug;53(8):1129-36.
PMID: 15247180
doi: 10.1136/gut.2003.036657.
Conclusions: These data demonstrate that elevated 1,25(OH)2D is more common in CD than previously appreciated and is independently associated with low bone mineral density. The source of the active vitamin D may be the inflamed intestine. Treatment of the underlying inflammation may improve metabolic bone disease in this subgroup of patients.
Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives.
Volvert ML, Seyen S, Piette M, Evrard B, Gangolf M, Plumier JC, Bettendorff L.
BMC Pharmacol. 2008 Jun 12;8:10.
PMID: 18549472
doi:10.1186/1471-2210-8-10
Conclusion
Our results show that, though benfotiamine strongly increases thiamine levels in blood and liver, it has no significant effect in the brain. This would explain why beneficial effects of benfotiamine have only been observed in peripheral tissues, while sulbutiamine, a lipid-soluble thiamine disulfide derivative, that increases thiamine derivatives in the brain as well as in cultured cells, acts as a central nervous system drug. We propose that benfotiamine only penetrates the cells after dephosphorylation by intestinal alkaline phosphatases. It then enters the bloodstream as S-benzoylthiamine that is converted to thiamine in erythrocytes and in the liver. Benfotiamine, an S-acyl derivative practically insoluble in organic solvents, should therefore be differentiated from truly lipid-soluble thiamine disulfide derivatives (allithiamine and the synthetic sulbutiamine and fursultiamine) with a different mechanism of absorption and different pharmacological properties.