title: Molecular mechanisms triggered by low-calcium diets.
abstract: Ca is not only essential for bone mineralisation, but also for regulation of extracellular and intracellular processes. When the Ca2+ intake is low, the efficiency of intestinal Ca2+ absorption and renal Ca2+ reabsorption is increased. This adaptive mechanism involves calcitriol enhancement via parathyroid hormone stimulation. Bone is also highly affected. Low Ca2+ intake is considered a risk factor for osteoporosis. Patients with renal lithiasis may be at higher risk of recurrence of stone formation when they have low Ca2+ intake. The role of dietary Ca2+ on the regulation of lipid metabolism and lipogenic genes in adipocytes might explain an inverse relationship between dairy intake and BMI. Dietary Ca2+ restriction produces impairment of the adipocyte apoptosis and dysregulation of glucocorticosteroid metabolism in the adipose tissue. An inverse relationship between hypertension and a low-Ca2+ diet has been described. Ca2+ facilitates weight loss and stimulates insulin sensitivity, which contributes to the decrease in the blood pressure. There is also evidence that dietary Ca2+ is associated with colorectal cancer. Dietary Ca2+ could alter the ratio of faecal bile acids, reducing the cytotoxicity of faecal water, or it could activate Ca2+-sensing receptors, triggering intracellular signalling pathways. Also it could bind luminal antigens, transporting them into mucosal mononuclear cells as a mechanism of immunosurveillance and promotion of tolerance. Data relative to nutritional Ca2+ and incidences of other human cancers are controversial. Health professionals should be aware of these nutritional complications and reinforce the dairy intakes to ensure the recommended Ca2+ requirements and prevent diseases.
authors.affiliation: Laboratorio de Metabolismo Fosfocálcico y Vitamina D Dr. F. Cañas, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Viviana
authors.initials: V
authors.lastname: Centeno
authors.forename: Gabriela Díaz
authors.initials: GD
authors.lastname: de Barboza
authors.forename: Ana
authors.initials: A
authors.lastname: Marchionatti
authors.forename: Valeria
authors.initials: V
authors.lastname: Rodríguez
authors.forename: Nori
authors.initials: N
authors.lastname: Tolosa de Talamoni
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D015992:Body Mass Index; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000172:deficiency / Q000378:metabolism; D002136:Calcium, Dietary / Q000008:administration & dosage / Q000378:metabolism*; D004032:Diet; D005260:Female; D006706:Homeostasis; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D007107:Immune System / Q000378:metabolism*; D007333:Insulin Resistance; D007413:Intestinal Mucosa / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D050356:Lipid Metabolism; D009369:Neoplasms / Q000209:etiology; D010024:Osteoporosis / Q000378:metabolism; D012307:Risk Factors; D015398:Signal Transduction
chemical_list: D002136:Calcium, Dietary; D006728:Hormones; D002118:Calcium