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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The (Ca2+ + Mg2+) ATPase which serves as a Ca2+ pump in the kidney basolateral membranes is essential to the maintenance of an intracellular Ca2+ concentration optimal for kidney function. Since atrial natriuretic peptide (ANP) is known to participate in the Ca2+ homeostasis mechanism, altered levels of ANP in diabetes may vary the pump activity and consequently the kidney function. In order to examine the modulatory role of ANP on (Ca2+ + Mg2+) ATPase in short- (6 weeks) and long-term (6 months) diabetes, rats were injected with streptozotocin (65 mg/kg body wt, i.v.). At 6 weeks, the plasma ANP was decreased whereas, ANP-receptor binding in the kidney basolateral membrane was increased. In contrast, there was an increased plasma ANP and decreased ANP receptor binding at 6 months. Insulin treatment to diabetic animals normalized these parameters. The (Ca2+ + Mg2+) ATPase activity was unchanged both at 6 weeks and 6 months. Our results demonstrate that the unchanged Ca2+ pump activity in short-term and long-term diabetes serves to maintain the Ca2+ homeostasis in the kidney cells and thus may maintain the hyperfiltration state in diabetes. Unaltered (Ca2+ + Mg2+) ATPase is achieved by the initial up-regulation and subsequent down-regulation of the ANP receptors.
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PMID:(Ca2+ + Mg2+) ATPase activity in kidney basolateral membrane in diabetes: role of atrial natriuretic peptide. 165

Diabetes mellitus caused significant reduction in serum testosterone and accessory sex glands weight. The sperm content of epididymal regions also decreased. Among the epididymal regions, the cauda epididymidal tissue alone showed significant reduction in Na(+)-K+ ATPase activity. However, Mg2+ ATPase activity was lowered in caput epididymidis only. Specific activity of Ca2+ ATPase significantly decreased in caput and cauda epididymides. All three ATPases decreased significantly in caput epididymidal spermatozoa leaving cauda epididymidal spermatozoa unaffected. Specific activity of alkaline phosphatase was suppressed in caput epididymidis and in the spermatozoa collected from caput and cauda epididymides, while the acid phosphatase was unaffected. In general, the results are suggestive of definite influence of diabetes on epididymal phosphatases which is region specific. Diabetes induced decrease in phosphatases may have an impact on secretory and absorptive functions of epididymis and thus on sperm maturation.
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PMID:Effect of diabetes mellitus on epididymal enzymes of adult rats. 166 46

Diabetes mellitus is associated with a significant reduction in the serum concentration of Mg2+. Several studies have suggested that hypomagnesemia may be implicated in the etiology of diabetic complications; however, no mechanism has been proposed. This study demonstrates that Mg2+ is a positive effector of inositol transport and is capable of promoting a 2.5-fold increase in the affinity of the transporter for inositol. Analysis of the kinetics of inositol transport shows that, at physiological concentrations of inositol, the reductions in Mg2+ concentrations that occur in diabetic patients would result in a significant decline in the rate of inositol transport (1.5- to 2-fold). We suggest that hypomagnesemia may be linked to the development of diabetic complications via reduction in the rate of inositol transport and subsequent intracellular inositol depletion. This assertion allows hypomagnesemia and the polyol theory to be unified into one mechanistic model for the development of diabetic complications.
Diabetes 1992 Jan
PMID:Effect of Mg2+ on Na(+)-dependent inositol transport. Role for Mg2+ in etiology of diabetic complications. 172 37

Red blood (RBC) ionized magnesium (Mg2+) was determined by nuclear magnetic resonance (NMR) in order to assess the usefulness of this technique as an index of magnesium depletion. Twenty-four normal subjects underwent a 3-week low-Mg diet. The RBC Mg2+ fell from 209 +/- 9.8 microM before diet to 162 +/- 9.3 microM at the end of the 3 weeks (p < 0.001). In patient populations, 22 hypomagnesemic hospitalized patients had a significantly lower RBC Mg than normal (146 +/- 7.1 microM, p < 0.002), and 37 outpatients with diabetes mellitus had a mean RBC Mg2+ of 172 +/- 7.1 microM which was also significantly lower than normal (p < 0.001). These data suggest that determination of RBC Mg2+ may be used to reflect intracellular Mg status.
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PMID:Determination of red blood cell intracellular free magnesium by nuclear magnetic resonance as an assessment of magnesium depletion. 184 44

Data suggest a critical role for Ca metabolism in the pathophysiology of hypertensive disease. Intracellularly, all hypertension displays elevated cytosolic free-Ca2+ and suppressed free-Mg2+ levels. Extracellularly, however, heterogeneous defects in Ca and Mg metabolism are observed. This apparent divergence may be explained by considering all hypertension as the expression, in varying degrees, of two underlying Ca-related mechanisms: one (salt sensitive, low renin, Ca(2+)-antagonist sensitive) dependent on inappropriate cellular Ca2+ uptake from the extracellular space and the other (salt insensitive, renin dependent, Ca(2+)-antagonist insensitive) dependent on increased cellular Ca2+ release from intracellular sites. Recent work highlights the role of 1,25-dihydroxyvitamin D3 and the newly described parathyroid hypertensive factor in volume-dependent low-renin forms of hypertension. Altered cellular ion handling may also explain metabolic and clinical correlates of hypertension, e.g., peripheral insulin resistance, hyperinsulinemia, obesity, and non-insulin-dependent diabetes mellitus (NIDDM). Thus, all subjects with NIDDM, whether hypertensive or not, display the same elevated cytosolic free-Ca2+ and suppressed free-Mg2+ levels observed in hypertension. Furthermore, adiposity, the level of blood pressure, and fasting and postglucose hyperinsulinemia are all closely and quantitatively related to intracellular free-Ca2+, free-Mg2+, and pH levels. This suggests a broader hypothesis, in which hypertension, obesity, insulin resistance, and NIDDM, each usually considered a distinct clinical entity, represent different clinical expressions of a common defect in cellular ion handling, hence explaining their frequent clinical coexistence in the general population.
Diabetes Care 1991 Jun
PMID:Calcium metabolism in hypertension and allied metabolic disorders. 186 22

Magnesium (Mg) deficiency in man may result in hypocalcemia, impaired PTH secretion, and low serum concentrations of 1,25-dihydroxyvitamin D [1,25-(OH)2D]. To determine whether these changes are due to selective Mg depletion, we studied 26 normal subjects before and after a 3-week low Mg (less than 1 meq/day) diet. This diet induced Mg deficiency, as demonstrated by a fall in pre- to postdiet serum Mg levels from 0.80 +/- 0.01 to 0.61 +/- 0.02 mmol/L (P less than 0.001), an increase in Mg retention from 11 +/- 4% to 62 +/- 4% (P less than 0.001), and a fall in red blood cell free Mg2+ from 205 +/- 10 to 162 +/- 7 microM (P less than 0.001). Serum calcium (Ca) fell significantly from 2.36 +/- 0.02 to 2.31 +/- 0.03 mmol/L (P less than 0.05), and serum 1,25-(OH)2D fell from 55 +/- 4 to 43 +/- 3 pmol/L (P less than 0.05). PTH secretion was impaired, as demonstrated by a fall or no change in serum PTH in 20 of 26 subjects despite a fall in the serum Ca and Mg. In addition, an iv injection of Mg in eight subjects after the diet resulted in a significant rise in PTH from 15 +/- 2 to 19 +/- 2 ng/L (P less than 0.01), whereas a similar injection given to six of the subjects before the diet resulted in a significant fall from 28 +/- 5 to 13 +/- 3 ng/L (P less than 0.001). The fall in serum 1,25-(OH)2D may be due to both the decrease in PTH secretion and a renal resistance to PTH. PTH resistance was suggested, as no increase in serum 1,25-(OH)2D was observed in the six subjects in which the PTH concentration rose by mean of 68% after the diet. Also, the rise in serum 1,25-(OH)2D after a 6-h human PTH-(1-34) infusion was significantly less after Mg deprivation. The results demonstrate that mild Mg depletion can impair mineral homeostasis and may be implicated as risk factor for osteoporosis in disorders such as chronic alcoholism and diabetes mellitus, in which Mg deficiency and osteoporosis are both common.
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PMID:Effect of experimental human magnesium depletion on parathyroid hormone secretion and 1,25-dihydroxyvitamin D metabolism. 193 21

Inositol 1,4,5-trisphosphate (IP3) increased the free-Ca2+ concentration in the incubation medium of permeabilized ob/ob mouse pancreatic islets. Spermine decreased the free-Ca2+ concentration through stimulation of mitochondrial Ca2+ uptake and attenuated the effect of IP3. Mg2+ antagonized the effects of spermine, thereby increasing the free-Ca2+ concentration and enhancing the effect of IP3 on the free-Ca2+ concentration. Because IP3 releases Ca2+ from endoplasmic reticulum, these results indicate that endoplasmic reticulum and mitochondria can interact in the regulation of the free-Ca2+ concentration in the cytosol of the pancreatic beta-cell.
Diabetes 1991 Mar
PMID:Effects of IP3, spermine, and Mg2+ on regulation of Ca2+ transport by endoplasmic reticulum and mitochondria in permeabilized pancreatic islets. 199 73

Pregnancy is marked by a state of hypomagnesemia. The serum magnesium level shows no gestational dependence (mean, 1.79 +/- 0.44 mg/dl) until 33 weeks, at which point it continuously declines. Serum magnesium is not depressed further with the onset of labor at term. Patients in preterm labor have a significantly depressed serum magnesium level (mean, 1.60 +/- 0.46 mg/dl; 21 to 33 weeks; p less than 0.0005). This level was not dependent on whether the etiology for the preterm labor was premature rupture of the membranes (PROM), twin gestation, abruption, placenta previa with bleeding, or chorioamnionitis. With PROM, the serum magnesium level was not depressed prior to the initiation of preterm labor. However, observation of hypomagnesemia for this and other etiologies just prior to the initiation of preterm labor were not available. Possible mechanisms by which hypomagnesemia induces uterine irritability are explored, including inhibition of adenyl cyclase with resultant increase in cytoplasmic calcium levels. Patients with diabetes mellitus appeared to have slightly reduced serum magnesium levels, but the results were not statistically significant. Magnesium levels in patients with preeclampsia were not significantly different from controls. Hypomagnesemia (magnesium 1.4 mg/dl or less) may be a marker for true preterm labor.
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PMID:Serum magnesium levels in pregnancy and preterm labor. 200 37

Incubation of basolateral membranes obtained from control rat kidney cortex in the presence of atrial natriuretic peptide (ANP) increased (Ca2+ + Mg2+) ATPase activity in a dose-dependent manner. Such response was absent in membranes obtained from animals made diabetic by streptozotocin injection (65 mg/kg, iv). The differential responses in the ATPase activity were not due to changes in the affinity for Ca2+ and insulin treatment in the diabetic animals completely reversed the situation. Our data suggest that ANP may mediate its cellular effects in part by changes in cellular Ca2+ homeostasis in kidney cortex and the lack of response of (Ca2+ + Mg2+) ATPase to ANP in chronic diabetes may contribute to the development of intracellular Ca2+ overload and nephropathy.
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PMID:Lack of response of (Ca2+ + Mg2+) ATPase to atrial natriuretic peptide in basolateral membranes from kidney cortex of chronic diabetic rats. 214 67

Myocardial triacylglycerol hydrolysis is subject to product inhibition. After hydrolysis of endogenous triacylglycerols, the main proportion of the liberated fatty acids is re-esterified to triacylglycerol, indicating the importance of fatty acid re-esterification in the regulation of myocardial triacylglycerol homoeostasis. Therefore, we characterized phosphatidate phosphohydrolase (PAP) and diacylglycerol acyltransferase (DGAT) activities, enzymes catalysing the final steps in the re-esterification of fatty acids to triacylglycerols in the isolated rat heart. The PAP activity was mainly recovered in the microsomal and soluble cell fractions, with an apparent Km of 0.14 mM for both the microsomal and the soluble enzyme. PAP was stimulated by Mg2+ and oleic acid. Oleic acid, like a high concentration of KCl, stimulated the translocation of PAP activity from the soluble to the particulate (microsomal) fraction. Myocardial DGAT had an apparent Km of 3.8 microM and was predominantly recovered in the particulate (microsomal) fraction. Both enzyme activities were significantly increased after acute streptozotocin-induced diabetes, PAP from 15.6 +/- 1.1 to 28.1 +/- 3.6 m-units/g wet wt. (P less than 0.01) and DGAT from 2.23 +/- 0.11 to 3.01 +/- 0.11 m-units/g wet wt. (P less than 0.01). In contrast with diabetes, low-flow ischaemia during 30 min did not affect PAP and DGAT activity in rat hearts. Perfusion with glucagon (0.1 microM) during 30 min did not affect total PAP activity, but changed the subcellular distribution. More PAP activity was recovered in the particulate fraction. DGAT activity was lowered by glucagon treatment from 0.37 +/- 0.03 to 0.23 +/- 0.02 m-unit/mg of microsomal protein (P less than 0.05). The role of PAP and DGAT activity and PAP distribution in the myocardial glucose/fatty acid cycle is discussed.
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PMID:Properties of phosphatidate phosphohydrolase and diacylglycerol acyltransferase activities in the isolated rat heart. Effect of glucagon, ischaemia and diabetes. 216 15


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