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Query: UMLS:C0028754 (obesity)
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In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.
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PMID:Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet. 183 14

Among renal stone formers with idiopathic hypercalciuria, patients who remain hypercalciuric despite low calcium intake have often been regarded as having a primary renal leak of calcium, i.e. renal hypercalciuria. However, at any given intake of calcium, dietary factors other than calcium can generate hypercalciuria, e.g. high intakes of sodium, of animal protein or of carbohydrates, or obesity itself. Thus, the incidence of renal hypercalciuria among stone formers has probably been overestimated. To address this issue, the aforementioned dietary and/or metabolic factors have been evaluated in 51 stone formers with idiopathic hypercalciuria refractory (i.e. U-Ca. V greater than 250 mg/24 h) to 5 days on low calcium intake (max. 400 mg/day). In 15 patients (all had U-Na. V greater than 200 mmol/24 h), U-Ca.V was within the 95% confidence limits of a nomogram U-Ca.V versus U-Na.V, suggesting that their idiopathic hypercalciuria was related, at least in part, to the high sodium intake. 7 patients had severe hyperuricosuria (greater than 1 g/24 h) suggesting high animal protein intake. 20 patients were obese (greater than 120% ideal weight) with (7 cases) or without (13 cases) concomitant fasting hyperinsulinemia (greater than 18 microU/ml). In addition, a careful retrospective analysis of intravenous pyelograms disclosed medullary sponge kidneys in 8 cases which had remained undiagnosed so far; in one of them histological confirmation was obtained after surgical removal of a renal pole and a radiologico-histological comparison. Thus, only 14 out of 51 patients had an otherwise unexplained idiopathic hypercalciuria on low calcium intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called "renal" idiopathic hypercalciuria most often has a dietary origin]. 334 5

Out of 89 stone formers with idiopathic hypercalciuria, 51 remained hypercalciuric on a low calcium diet over 5 days: a renal leak of calcium could thus have been suspected in them. Dietary factors such as high sodium or high animal protein intake, and metabolic factors such as obesity with or without hyperinsulinemia, which all might account for the hypercalciuria of these patients, have been evaluated. This evaluation revealed conditions known to be associated with hypercalciuria in 37 of these 51 patients: 15 had hypercalciuria related to a high sodium intake, 7 had severe hyperuricosuria (greater than 1 g/24 h) reflecting a high animal protein intake, 20 were obese (greater than 120% of ideal weight) with (7 cases) or without (13 cases) concomitant high fasting plasma level of insulin (greater than 18 microU/ml). A careful retrospective analysis of the intravenous pyelograms disclosed medullary sponge kidneys in 8 cases which had remained undiagnosed so far. One of them was studied histologically. Only 14 out of 51 patients had an otherwise unexplained hypercalciuria on a low calcium diet. It is concluded that dietary causes appear to play a key role in 'idiopathic' hypercalciuria, that the incidence of a primary renal leak of calcium among idiopathic stone formers is much smaller than initially thought, and that this condition can hide unrecognized medullary sponge kidneys.
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PMID:Dietary factors and medullary sponge kidneys as causes of the so-called idiopathic renal leak of calcium. 368 38

The calciuric response and the changes of plasma glucose and insulin produced by a 75-gram oral glucose tolerance test were determined in 27 male patients with idiopathic calcium renal stones (6 with dietary hypercalciuria, 5 with nondietary hypercalciuria and 16 with normocalciuria) and 22 healthy male subjects. The subjects were classified as obese (> or = 120% ideal weight) and nonobese. The incidence of an abnormal response to glucose loading was similar in the stone patients and the healthy subjects. In addition, the plasma glucose and insulin levels after oral glucose load did not differ between the stone patients and control subjects and were affected by the individual degree of obesity. Urinary calcium excretion increased significantly after glucose ingestion in both the stone patients and the control subjects. Urinary calcium excretion was greater in the stone patients than in the control subjects due to the presence of patients with nondietary hypercalciuria, and the increment in urinary calcium excretion in the dietary hypercalciuric and normocalciuric stone patients was indistinguishable from that in the control subjects. The degree of obesity did not affect the increment in urinary calcium excretion. These results suggest that overconsumption of refined carbohydrates such as sugar-sweetened soft drinks, soda and cakes may be a risk factor for stone formation, especially in the patients with nondietary hypercalciuria.
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PMID:Glucose metabolism in renal stone patients. 826 8

We studied the prevalence of a history of nephrolithiasis in first- and second-degree relatives of 74 children with hypercalciuria (HC), 61 with hyperuricosuria (HU), and 41 with HC plus HU, and in a control population of 261 children with different diseases. Family history of nephrolithiasis was found in 69% of HC, 75% of HU, 78% of HC plus HU, and 22% of control patients. The prevalence was not different among HC, HU, and HC plus HU groups, but was significantly higher in each study group than the control group (P=0.0001). Body mass index >95th percentile was found in only 4.7% of the patients with HC or HC plus HU. Calculi (>3 mm in diameter) were present in 8.9% of the patients with a family history of nephrolithiasis and in 9.4% of those with no family history (P=0.85). Microcalculi (<3 mm in diameter) were found by sonography in 56.6% of the patients with and in 53.3% of those without a family history of nephrolithiasis (P=0.83). Children with HC and/or HU have a strong familial prevalence of nephrolithiasis. Obesity does not seem to affect the association of familial nephrolithiasis and hypercalciuria in children. The presence of nephrolithiasis in families of children with HC and/or HU is not associated with a higher rate of formation of calculi or microcalculi.
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PMID:Idiopathic hypercalciuria and hyperuricosuria: family prevalence of nephrolithiasis. 1104 95

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.
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PMID:Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure. 1272 57

Both diabetes and fractures affect a large proportion of older adults. Recent cohort studies indicate that diabetes itself is associated with increased risk of fracture of the hip, proximal humerus, and foot. Observational studies and animal models suggest that decreased bone strength in diabetes may contribute to fracture risk but this remains a controversial issue. Type 1 diabetes is associated with modest reductions in bone mineral density (BMD) but type 2 diabetes is often characterized by elevated BMD. This paradox of higher BMD but increased fracture risk in type 2 diabetes may be explained by a combination of more frequent falls and poorer bone quality. Diabetes can impact bone through multiple pathways, some with contradictory effects, including obesity, changes in insulin levels, higher concentrations of advanced glycation end products in collagen, hypercalciuria associated with glycosuria, reduced renal function, lower insulin-like growth factor-I, microangiopathy, and inflammation. A better understanding of how diabetes metabolism and treatments affect bone would improve fracture prevention efforts in older diabetic adults.
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PMID:Diabetes Mellitus: Does it Affect Bone? 1451 15

Diabetes mellitus and osteoporosis are chronic diseases with an elevated and growing incidence in the elderly. Recent epidemiological studies have demonstrated an elevated risk of hip, humerus and foot fractures in elder diabetic subjects. While type 1 diabetes is generally associated with a mild reduction in bone mineral density (BMD), type 2 diabetes, more prevalent in old subjects, is frequently linked to a normal or high BMD. Studies on experimental models of diabetes have suggested an altered bone structure that may help to explain the elevated risk of fractures observed in these animals and may as well help to explain the paradox of an incremented risk of fractures in type 2 diabetic elderly in the presence of normal or elevated BMD. In addition, diabetic elderly have an increased risk of falls, consequent at least in part to a poor vision, peripheral neuropathy, and weaken muscular performance. Diabetes may affect bone tissue by different mechanisms including obesity, hyperinsulinemia, deposit of advanced glycosilation end products in collagen fibre, reduced circulating levels of IGF-1, hypercalciuria, renal function impairment, microangiopathy and chronic inflammation. A better understanding of these mechanisms may help implement the prevention of fractures in the growing population of mature diabetics.
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PMID:[Osteoporosis and diabetes]. 1564 75

Urolithiasis is a multifactorial recurrent disease of world-wide distribution in rural, urban, industrial and non-industrial regions. Changes in urinary pH is a risk factor especially with hyperuricosuria, hypercalciuria or hyperoxaluria. With recurrence, hypercalcuria and higher urinary oxalate levels are more frequent. Hypercalciuria and hyperuricosuria showed correlation with family history of stones. The ionic relations between various stone forming salts in urine of patients are opposite to that in controls and are well represented in stone composition. Obesity is a risk factor in both genders. Over eating a diet rich in all nutrients was associated with hyperuricosuria while a diet high only in fat was associated with other urinary disturbances. High protein and fat intake are risk factors. High or low calcium diet was associated with urolithiasis and supplemental calcium is not a risk factor. Potassium and magnesium citrate are potent in inhibiting the growth of stone fragments after extracorporeal shock wave lithotripsy. Whether in patients or normal subjects, drinking hard water should be avoided; tap water or low calcium content water is preferable. Seasonal variations in temperature affected urinary volume, pH and relative saturation of uric acid. To prevent recurrence, patients should maintain high fluid intake achieving a urine volume of 2 liters per day.
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PMID:Urolithiasis in adults. Clinical and biochemical aspects. 1595 54

The polyol isomalt (Palatinit) is a well established sugar replacer. The impact of regular isomalt consumption on metabolism and parameters of gut function in nineteen healthy volunteers was examined in a randomised, double-blind, cross-over trial with two 4-week test periods. Volunteers received 30 g isomalt or 30 g sucrose daily as part of a controlled diet. In addition to clinical standard diagnostics, biomarkers and parameters currently discussed as risk factors for CHD, diabetes or obesity were analysed. Urine and stool Ca and phosphate excretions were measured. In addition, mean transit time, defecation frequency, stool consistency and weight were determined. Consumption of test products was affirmed by the urinary excretion of mannitol. Blood lipids were comparable in both phases, especially in volunteers with hyperlipidaemia, apart from lower apo A-1 (P=0.03) for all subjects. Remnant-like particles, oxidised LDL, NEFA, fructosamine and leptin were comparable and not influenced by isomalt. Ca and phosphate homeostasis was not affected. Stool frequency was moderately increased in the isomalt phase (P=0.006) without changes in stool consistency and stool water. This suggests that isomalt is well tolerated and that consumption of isomalt does not impair metabolic function or induce hypercalciuria. In addition, the study data indicate that isomalt could be useful in improving bowel function.
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PMID:Effects of isomalt consumption on gastrointestinal and metabolic parameters in healthy volunteers. 1619 83


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