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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Embryos of Xenopus laevis reared in media with various low (less than or equal to 10(-5) M) magnesium ion concentrations will exhibit differing degrees of a potentially lethal magnesium starvation syndrome depending on the ion concentration and rearing temperature. The higher the rearing temperature or the lower the magnesium ion content of the medium the more severely the syndrome will be expressed. (Normal development can be expected at temperatures 13-30 degrees C and magnesium ion concentrations greater than 10(-5)M to 10(-2) M.). The magnesium deficiency syndrome in Xenopus embryos is described in detail and compared with the normal and anucleolate conditions. The deficiency condition becomes manifest after hatching as retarded growth and differentiation with progressive paralysis and edema. At the same time alterations are observed in the pattern of soluble proteins. The use of magnesium ions as a probe for investigating developing systems is discussed.
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PMID:Magnesium deficiency in embryos of Xenopus laevis. 88 66

Obesity is characterized by a high risk for glucose intolerance and cardiovascular disease. Since magnesium deficiency or depletion have often been associated with both pathologies, is of interest to study magnesium status in severely obese subjects before any form of treatment. Negative magnesium balances have been described in overweight persons submitted to total starvation, hypocaloric diets, and obesity surgery. For this reason 80 non-diabetic obese men and 118 age-matched obese women were studied. Serum and erythrocyte magnesium concentrations were significantly higher in the male population but the mean values were not suggestive of a magnesium deficit before any form of treatment was started. Since metabolic abnormalities and cardiovascular risk are greater in patients with upper body fat distribution (UBFD) both sexes were subdivided according to "waist-to-hip" circumference ratio. No difference could be shown in the obese men but in women, UBFD subjects showed higher basal insulin levels and increased erythrocyte magnesium concentration as compared to those with classical gynoid fat distribution. A 75 g oral glucose tolerance test enabled the subjects to be subdivided into those with normal or impaired glucose tolerance (IGT). The IGT group in both sexes was older and more obese. Mean values of serum magnesium and erythrocyte magnesium were not decreased despite the more pronounced insulin resistance in the IGT group. However a significant negative correlation was found between fasting blood sugar/insulinaemia and erythrocyte magnesium, showing that this middle-aged obese population can maintain normal circulating levels of magnesium, in contrast to type II diabetics or older subjects where for other reasons (urinary losses or decreased intake) magnesium status is interfered with.
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PMID:Magnesium and obesity: influence of gender, glucose tolerance, and body fat distribution on circulating magnesium concentrations. 146 56

The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.
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PMID:Magnesium deficiency. Causes and clinical implications. 649 96

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Although the symptoms of magnesium deficiency are well documented in plants, the primary physiological effects of low Mg availability remain largely unknown. This paper describes the physiological responses of Mg starvation in Arabidopsis thaliana. Growth characteristics, Mg and sugar concentration, and photochemical performance were measured at regular intervals during the induction of Mg deficiency. These data show that Mg deficiency increased the sugar concentration and altered sucrose export from young source leaves before any noticeable effect on photosynthetic activity was seen. The decline in photosynthetic activity might be elicited by increased leaf sugar concentrations. Transcript levels of Cab2 (encoding a chlorophyll a/b protein) were lower in Mg-deficient plants before any obvious decrease in the chlorophyll concentration. These transcriptional data suggest that the reduction of chlorophyll is a response to sugar levels, rather than a lack of Mg atoms for chelating chlorophyll.
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PMID:Physiological characterization of Mg deficiency in Arabidopsis thaliana. 1598 14