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PubMed1984

Effect of insulin treatment on the susceptibility of the diabetic rat to Escherichia coli-induced pyelonephritis.

Escherichia coli-induced pyelonephritis was studied in untreated alloxan-diabetic rats, insulin-treated diabetic rats, glucose water-drinking (diuresing) nondiabetic rats, and tap water-drinking (nondiuresing) nondiabetic rats following injection of E. coli either into the emptied urinary bladder, into the left kidney, or intravenously. For prevention of an ascending infection in the right kidney, the right ureter was ligated and transected immediately prior to bladder or intrarenal inoculation. These experiments established that in normal rats ascending renal infection alone occurred following introduction of small inocula into the bladder--and then only when facilitated by diuresis. In diabetic rats both ascending and hematogenous renal infection occurred following introduction of small inocula into the bladder. Insulin treatment that reduced hyperglycemia also reduced glycosuria and restored urinary antibacterial activity against small inocula of E. coli but only partially reduced polyuria and prevented hematogenous but not ascending infection. Thus, hyperglycemia was probably the major factor promoting hematogenous renal infection, whereas polyuria--and therefore vesicoureteral reflux--was the major factor promoting ascending infection.

Animals↗

PubMed1988

Exocrine pancreatic enzyme activities and mineral concentrations in SHR/N-corpulent (cp) male rats.

Exocrine pancreatic enzyme activities and mineral concentrations were measured in a newly developed congenic strain of corpulent rat (SHR/N-cp). Approximately 4- to 5-wk-old corpulent (cp/cp) and lean (+/?) male rats consumed a diet containing 54% carbohydrate as either cooked cornstarch or 27% cooked cornstarch and 27% fructose for 9.5 mo. After consuming the diet for 3 mo, corpulent rats were hyperinsulinemic, hyperlipidemic and exhibited glycosuria. After consuming the diet for 9.5 mo corpulent rats were twofold heavier and pancreatic weight was 77% that of their lean littermates. Corpulent rats that consumed starch exhibited lower total pancreatic protein with no significant change in total DNA and RNA. In the corpulent rat, both lipase- and chymotrypsinogen-specific activities and both the specific activities and the content of amylase or trypsinogen were lower than those of lean littermates. Fructose consumption resulted in lower pancreatic copper and iron concentrations, and zinc concentration was elevated in corpulent rats. This study suggests that the SHR/N-corpulent rat may be a useful model for studying exocrine pancreatic function in insulin-independent diabetes.

Amylases↗

PubMed1997

Chinese herbs nephropathy presentation, natural history and fate after transplantation.

BACKGROUND: Chinese herbs nephropathy is a new type of subacute interstitial nephropathy reported in women who had followed a slimming regimen including Chinese herbs. METHODS: We report the clinical presentation and follow-up of 15 cases and compare them with a control group of 15 women with interstitial nephropathies of other origins, matched for age, sex, and initial serum creatinine (mean 3 mg/dl). RESULTS: At presentation the Chinese herbs nephropathy group differed from the control group by a lower proteinuria (P = 0.009), a more severe anaemia (P = 0.002), and a higher prevalence of aortic insufficiency (42% vs 0%, P < 0.05). It was further characterized by mild hypertension in 80%, glycosuria and leukocyturia in 40% and asymmetric kidneys in 54% of the cases. During follow-up, deterioration of renal function was faster in the Chinese herbs nephropathy than in the control group (P < 0.05). It was influenced by the duration of Chinese herbs treatment (P = 0.037) and the delay between the end of Chinese herbs ingestion and diagnosis of the disease (P = 0.013). In three cases, renal failure developed 3 years after Chinese herbs ingestion. Complications included severe aortic regurgitation requiring surgery (n = 1), urothelial carcinoma (n = 2), bilateral ureterohydronephrosis due to periureteral fibrosis (n = 1). Five patients with Chinese herbs nephropathy were successfully transplanted, without evidence of recurrence of the disease. CONCLUSIONS: Chinese herbs nephropathy is characterized by a lower proteinuria, more severe anaemia, and a faster progression to renal failure than other interstitial nephropathies. The duration of Chinese herbs treatment and interval between withdrawal of Chinese herbs and diagnosis are correlated with the rate of progression. Severe, unusual extrarenal complications may affect Chinese herbs nephropathy patients.

Adult↗

PubMed2001

Acute, subacute, and subchronic oral toxicity studies of 1,1-dichloroethane in rats: application to risk evaluation.

1,1-Dichloroethane (DCE) is a solvent that is often found as a contaminant of drinking water and a pollutant at hazardous waste sites. Information on its short- and long-term toxicity is so limited that the U.S. EPA and ATSDR have not established oral reference doses or minimal risk levels for the volatile organic chemical (VOC). The acute oral LD(50) in male Sprague-Dawley (S-D) rats was estimated in the present study to be 8.2 g/kg of body weight (bw). Deaths appeared to be due to CNS depression and respiratory failure. In an acute/subacute experiment, male S-D rats were given 0, 1, 2, 4, or 8 g DCE/kg in corn oil by gavage for 1, 5, or 10 consecutive days. The animals were housed in metabolism cages for collection of urine and sacrificed for blood and tissue sampling 24 h after their last dose. There were decreases in body weight gain and relative liver weight at all dosage levels, as well as increased renal nonprotein sulfhydryl levels at 2 and 4 g/kg after 5 and 10 days. Elevated serum enzyme levels, histopathological changes, and abnormal urinalyses were not manifest. For the subchronic study, adult male S-D rats were gavaged with 0.5, 1, 2, or 4 g DCE/kg 5 times weekly for up to 13 weeks. Animals receiving 4 g/kg exhibited pronounced CNS depression, with more than one-half dying by week 11. The 2-g/kg rats exhibited moderate CNS depression. One 2-g/kg rat died during week 6. There were very few manifestations of organ damage in animals that succumbed or in survivors at any dosage level. Decreases in bw gain and transient increases in enzymuria were noted at 2 and 4 g/kg. Serum enzyme levels and blood urea nitrogen were not elevated, nor were glycosuria or proteinuria present. Chemically induced histological changes were not seen in the liver, kidney, lung, brain, adrenal, spleen, stomach, epididymis, or testis. Hepatic microsomal cytochrome P450 experiments revealed that single, high oral doses of DCE did not alter total P450 levels, but did induce CYP2E1 levels and activity and inhibit CYP1A1 activity. These effects were reversible and regressed with repeated DCE exposure. There was no apparent progression of organ damage during the 13-week subchronic study, nor appearance of adverse effects not seen in the short-term exposures. One g/kg orally (po) was found to be the acute, subacute, and subchronic LOAEL for DCE, under the conditions of this investigation. In each instance, 0.5 g/kg was the NOAEL.

Acetylglucosamine↗

PubMed2002

Nephrotoxicity of chlorofluoroacetic acid in rats.

Dichloroacetic acid (DCA), chlorofluoroacetic acid (CFA), and difluoroacetic acid (DFA) are inhibitors of pyruvate dehydrogenase kinase. DCA is used for the clinical management of congenital lactic acidosis. Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1. In rodents, DCA causes multiorgan toxicities and is hepatocarcinogenic. The toxic effects of CFA, which is an excellent substrate but a poor inactivator of GSTZ1-1, have not been investigated. The objective of this study was to investigate the nephrotoxicity of CFA. Rats given a single dose of 1.5 mmol/kg CFA became anuric and died within 24 h. Urinalysis and light microscopic analysis showed that rats given 0.6-1.2 mmol/kg CFA developed polyuria, glycosuria, and renal proximal tubular damage. Electron microscopic analysis indicated a role for apoptosis in CFA-induced cell death. The nephrotoxicity of CFA was associated with a dose-dependent increase in inorganic fluoride excretion. Treatment of rats with DCA for 5 days to inactivate GSTZ1-1 failed to prevent metabolism of CFA to fluoride and did not block CFA-induced renal damage. A role for GSTZ1-1-catalyzed release of fluoride from CFA is proposed but a role for other enzymes cannot be excluded. DFA, which is not metabolized to fluoride by GSTZ1-1, was given to rats as a control and was also nephrotoxic: rats given 1.2 mmol DFA/kg/day for 5 days had normal urine volumes but showed proximal and distal tubular damage; fluoride excretion was not elevated. The mechanism of DFA-induced nephrotoxicity is not known but appears to differ from that of CFA.

Acetates↗

PubMedDate not supplied

Hyperuricosuria in the Fanconi syndrome.

A patient with asymptomatic adult Fanconi syndrome with glycosuria, amino-aciduria, hypophosphatemia, and renal tubular acidosis was found to have hypouricemia (serum uric acid, 1.5-1.8 mg/100 ml) secondary to increased renal clearance of urate (urate clearance/glomerular filtration rate, 32 per cent). Increased urate clearance in this patient with multiple reabsorptive defects probably represents diminished urate reabsorption. Consistent with this, the uricosuric response to probenecid was diminished. Reabsorption of filtered urate appeared to be intact. Inhibition of urate secretion with pyrazinamide completely suppressed the uricosuria in this patient, suggesting that increased urate clearance was due to either enhanced secretion or diminished reabsorption of secreted urate. There was no direct evidence for increased urate secretion. The response of urate excretion to pharmacologic inhibitors of tubular transport of urate differs in various clinical states associated with hyperuricosuria. The responses may reflect different mechanisms of hyperuricosuria.

Fanconi Syndrome↗

PubMedDate not supplied

Renin-angiotensin-aldosterone system, electrolyte homeostasis and blood pressure in alloxan diabetes.

The effect of a chronic glucose osmotic diuresis on electrolyte homeostasis was evaluated in alloxan diabetic rats with urine volumes greater than 150 ml/day and glycosuria of 4 to 10 gm/day. Results were compared with control rats for periods up to 84 days. Sodium and potassium intake and urinary losses were significantly higher in diabetic animals throughout the study periods. Negative Na balance, however, persisted for only four days, and negative K balance for only 18 days. Blood volumes were elevated probably secondary to the osmotic effect of hyperglycemia (serum glucose greater than 600 mg %). Plasma renin activity decreased progressively, in part because of an early decrease in renin substrate at a time when renin concentration was normal. Despite hyperkalemia, mean plasma aldosterone was not increased compared with that in control rats, suggesting diabetic rats had relative hypoaldosteronism. Although three diabetic rats became hypertensive, no significant difference in mean blood pressure was observed between the groups. The results suggest that diabetic rats have losses of Na and K early in their diabetes, following which mechanisms to conserve Na and K are activated preventing further electrolyte depletion despite continuation of the osmotic diuresis. Decreased renin activity with inadequate stimulation of aldosterone would contribute to K conservation. Maintenance of Na balance must be explained by increased Na intake and other renal Na conserving mechanisms.

Aldosterone↗

PubMed2005

An unusual cause of hypokalemic paralysis: aristolochic acid nephropathy with Fanconi syndrome.

Aristolochic acid nephropathy (AAN) with Fanconi syndrome presenting as hypokalemic paralysis is extraordinarily rare and may be unrecognized. We describe a 41-year-old man who presented with the inability to ambulate upon awakening in the morning. Physical examination revealed symmetric paralysis of bilateral lower limbs. Laboratory studies showed profound hypokalemia with renal potassium (K) wasting, hyperchloremic metabolic acidosis, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, and glycosuria, consistent with Fanconi syndrome. Mild renal insufficiency was also observed. A meticulous search for underlying causes of Fanconi syndrome was unrevealing. However, a significant amount of aristolochic acid (AA) was detected in the consumed Chinese herb mixture (AA-I, 7 microg/g) for the treatment of his leg edema for the past 2 months. His hypokalemia, renal insufficiency, and Fanconi syndrome completely resolved 2 months after the withdrawal of Chinese herb mixture and the supplementation of potassium citrate and active vitamin D3. AAN with Fanconi syndrome should be considered as a cause of hypokalemia in any patient administered undefined Chinese herbs.

Adult↗

PubMed1981

Impaired wound healing in streptozotocin diabetes. Prevention by supplemental vitamin A.

Goodson and Hunt showed that wound healing is impaired in streptozotocin (Sz) diabetic rats; we speculated that this impairment results from defective early inflammatory responses to wounding. Because we had shown that supplemental vitamin A stimulates the early inflammatory response to wounding in nondiabetic rats, we studied the effect of supplemental vitamin A on wound healing in rats with Sz-induced diabetes. Male Sprague-Dawley rats were fed a commercial rat chow containing twice the amount of vitamin A recommended by the NRC for healthy rats. The rats ate and drank (tap water) ad libitum. Two-thirds of the rats were injected (intravenously) with Sz 60 mg/kg body weight. All of these rats became diabetic (hyperglycemia greater than 350 mg/dl, hyperphagic, polydipsic, polyuric, glycosuric greater than 2%). Seven days later, half of the Sz-injected rats were continued on the chow (Group 2) while the other half (Group 3) were switched to the chow supplemented with 150,000 units of vitamin A/kg chow. The next day, all were wounded (7 cm skin incisions and s.c. polyvinyl alcohol sponge implants). Similarly wounded saline injected nondiabetic rats ingesting the unsupplemented chow served as controls (Group 1). The wounds of Group 2 rats healed poorly compared to Group 1 (breaking strength of skin incisions, 308 +/- 19 g vs 584 +/- 23 g, p less than 0.001; hydroxyproline of the sponge reparative tissue, 0.87 mg vs 2.40 mg/100 mg sponge p less than 0.001). Supplemental vitamin A (Group 3) did not affect the hyperglycemia, hyperphagia, polydipsia or glycosuria, but increased the breaking strengths of the incisions of the diabetic rats (468 +/- 40 g, p less than 0.001), and the sponge hydroxyproline (2.38 mg/100 mg sponge, p less than 0.001). In another experiment, in which the wounding and start of supplemental vitamin A were delayed until 28 days after streptozotocin administration (50 mg/kg body weight), similar results were obtained. Streptozotocin diabetes also caused a decrease in the cross-linking of reparative collagen as judged by the ratio of breaking strengths of skin incisions before and after formalin fixation. Supplemental vitamin A did not influence this defect. Sz also caused peripheral lymphocytopenia, adrenal hypertrophy and thymic involution which responded to the supplemental vitamin A. Based upon experimental data and theoretical considerations we conclude Sz diabetes causes two defects in wound healing: a) quantitatively (reduction in reparative collagen accumulation) and b) qualitative reduction in the degree of cross-linking of reparative wound collagen. The action of supplemental vitamin A in correcting the impaired wound healing, adrenal enlargement, thymic involution and lymphocytopenia of Sz-diabetic rats is independent of an effect on their disturbed carbohydrate metabolism.

Animals↗

PubMed1998

Indinavir-associated lipodystrophy.

BACKGROUND: Lipodystrophies are rare cutaneous disorders characterized by the symmetrical loss of subcutaneous fat from the body surface. The cause of lipodystrophy is not known, but a possible genetic predisposition is likely and either overt diabetes mellitus or insulin resistance are often associated. DESIGN AND METHODS: Case study. PATIENTS: Eight patients who developed either partial or generalized lipodystrophy after protease inhibitor therapy. RESULTS: In all eight patients lipodystrophy occurred after 2-12 months of starting indinavir and was not preceded by weight loss or inflammatory skin disease. Short-term follow-up after withdrawal of therapy showed no change in the patients' appearance. One patient developed glycosuria as lipodystrophy became manifest. In three cases glucose tolerance test was performed revealing a high level of insulin between the first and third hour of loading. CONCLUSIONS: In our view, lipodystrophy is an unwanted side-effect of protease inhibitor therapy causing noticeable disfigurement.

Adult↗

PubMedDate not supplied

Hypothalamic responsiveness in DOCA hypertensive rats augmented by streptozotocin-induced diabetes.

In rats with deoxycorticosterone acetate (DOCA) salt hypertension, induction of diabetes with streptozotocin did not aggravate the elevation in blood pressure, but pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were enhanced. Along with glycosuria and hyperglycemia, the other effects of streptozotocin-induced diabetes were: reduced body weight, increased fluid intake, and bradycardia. Despite enhanced responsiveness to hypothalamic stimulation, blood pressure increases produced by intravenous injections of norepinephrine, tyramine, or vasopressin were unaltered. When pressor responses were compared in diabetic rats drinking either tap water or isotonic saline solution, no appreciable differences occurred. It was considered possible that hypothalamic responsiveness was enhanced in diabetic-DOCA hypertensive rats by increases not only in sympathetic nerve firing but also in release of endogenous norepinephrine.

Animals↗

PubMed1998

Effect of long-term treatment with enalapril in streptozotocin diabetic and DOCA hypertensive rats.

We studied the effects of long-term treatment with enalapril (5 mg/kg/day orally) on various biochemical and cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosterone acetate (DOCA) hypertensive rats. Female Wistar rats made diabetic or hypertensive or both by streptozotocin (STZ; 45 mg/kg) or deoxycorticosterone acetate (DOCA; 10 mg/kg, p.o., daily) or both. Enalapril (5 mg/kg) was administered daily by the oral route for 6 weeks. At the end of 6 weeks, blood samples were taken to analyze glucose, insulin, and lipids. Blood pressure and heart rate were recorded by a noninvasive technique, and cardiac functions were recorded by Neely's working heart preparation. Injection of STZ produced severe glycosuria (>2%), hyperglycemia, hypoinsulinemia, and loss of body weight. It also produced hypercholesterolemia, hypertriglyceridemia, hypertension, bradycardia, and decreased left ventricular developed pressure (LVDP) and increase in angiotensin-converting enzyme (ACE) in left ventricular tissue. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in nondiabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment with enalapril prevented an increase in the blood pressure and the heart weight. Decrease in the heart rate, reduction in LVDP, and increase in intracardiac activity were observed in diabetic rats; these were also prevented by enalapril treatment. Enalapril had no effect on plasma glucose and did not modify plasma insulin levels in diabetic animals. The effects of STZ and DOCA together were not additive on the investigated parameters, and enalapril was similarly efficient in diabetic and diabetic hypertensive animals.

Analysis of Variance↗

PubMedDate not supplied

Improving the care of women with gestational diabetes.

The article reviews gestational diabetes mellitus, including etiology, diagnostic and screening criteria, risk factors, and care of the affected woman. Gestational diabetes mellitus affects approximately 7% of all pregnant women, resulting in more than 200,000 cases each year, and is defined as glucose intolerance that begins or is first recognized during pregnancy. Women are considered at high risk for gestational diabetes if they are markedly obese, have a personal history of gestational diabetes, have a strong family history of diabetes, or have glycosuria. Risk assessment is essential in determining whether a woman should be screened or tested for gestational diabetes. Women who have had gestational diabetes should have comprehensive preconception care prior to a subsequent pregnancy to ascertain appropriate weight, nutrition, exercise, and signs of gestational diabetes.

Aftercare↗

PubMed1986

Responses of pancreatic b cells to alloxan and streptozotocin in the guinea pig.

Guinea pigs injected with streptozotocin were significantly hyperglycemic on day 1 after injection but only mildly so on day 14. However, serum insulin levels were significantly depressed on day 14; at this time the animals had lost 25% of their initial body weights and were severely glycosuric. The volume fraction of immunostainable B cells in the pancreas was reduced to one third of control values by day 1 after injection and remained at this level by day 14. Animals that received alloxan were slightly hyperglycemic on day 1 but not day 14. Both serum insulin and volume fraction of B cells in the pancreas were reduced by 70% on day 1 but had returned to control levels by day 14. Body weights for this group were equivalent to controls at both time points. These data indicate that: streptozotocin treatment of guinea pigs causes a diabetes-like condition characterized by insulin deficiency, pancreatic B cell loss, glycosuria, and weight loss, which are not reversed in the first 2 weeks after injection, whereas hyperglycemia is only transitory; alloxan also produces a diabetes-like condition early after injection, but all signs of diabetes disappear within 2 weeks, by which time serum insulin levels and the volume fraction of B cells in the pancreas have returned to normal. The experimental results suggest that regeneration of islet B cells following destruction by alloxan may be the primary cause of the recovery of alloxan-injected guinea pigs from the effects of the drug, whereas the persistence of insulin deficiency is consistent with an absence of islet B cell regeneration in the streptozotocin-treated animals.

Alloxan↗

PubMed1990

Diabetic strain (WBN/Kob) of rat characterized by endocrine-exocrine pancreatic impairment due to distinct fibrosis.

A spontaneously developed endocrine-exocrine pancreatic dysfunction was observed in the aged males of an inbred strain of Wistar rats, WBN/Kob. Nonobese male WBN/Kob rats developed glycosuria and hyperglycemia at around 9 months of age. Cumulative incidence of diabetes in male rats was 43% (33 of 76) at 12 months of age and reached 90% at the age of 21 months. In contrast, female rats did not become diabetic. Urinary excretion of amylase in WBN/Kob rats was significantly increased in comparison with control Wistar rats. Moreover, the exocrine pancreatic function test was impaired in WBN/Kob rats. Pathological examination of pancreata revealed infiltration of inflammatory cells, hemorrhage, deposition of hemosiderin, and fibrinous exudation around pancreatic ducts and blood vessels at 3 months of age. A gradual increase of fibrous tissue into the exocrine tissue and islets was observed with advancing age. The extremely enlarged interlobular lymph nodes were also observed. At the age of 12 months, the fibrous tissue replaced extensive areas of the pancreas and involved islets. The amylase content of pancreata in WBN/Kob rats was markedly decreased in comparison with that in Wistar rats at 12 months of age. Islets composed of few endocrine cells were detected. Immunohistochemical staining for insulin and glucagon showed a decreased number of not only B cells but also A cells. Moreover, both the pancreatic insulin and glucagon contents were markedly decreased in WBN/Kob rats in comparison with Wistar rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amylases↗

PubMed1994

Relation between pancreatic islet cellular infiltration and plasma fibrinogen or alpha 1-acid glycoprotein levels in spontaneously and streptozotocin-diabetic rats: an increase in these protein levels is not necessary for inducing microcirculatory erythrocyte velocity alteration.

Plasma levels of fibrinogen, alpha 1-acid glycoprotein (AG) and albumin, pancreatic insulitis quantitative scores, and erythrocyte velocity in the mesoappendix microvessels were measured in BB diabetic (BBD) and streptozotocin-diabetic rats (WSTZ) in order to answer the following questions: (a) Does hyperfibrinogenemia or increase in AG plasma level occur in BBD and WSTZ rats, and if so, are these alterations secondary to the hyperglycemia or to an inflammatory process such as insulitis? (b) Is there a decrease in microcirculatory flow in the BBD and WSTZ rats, and if so, is it secondary to the hyperfibrinogenemia and/or the hyperglycemia? Insulitis was present in the BBD rats after 5 weeks of disease (with a score of 2.9 +/- 0.1 vs. 1.4 +/- 0.6 in the normoglycemic controls), but absent in WSTZ rats after 5 months of disease (1.2 +/- 0.06 vs. 1.1 +/- 0.06). Increase in fibrinogen and AG plasma levels was observed in the BBD rats only and appears linked to the insulitis. The major acute phase protein AG level is increased in BBD rats already on the first day of appearance of glycosuria. In the WSTZ rats, without insulitis, chronic hyperglycemia alone did not induce an increase in fibrinogen and AG plasma levels. A decreased microcirculatory erythrocyte velocity has been found in both BBD and WSTZ rats. Thus an increase in fibrinogen or AG plasma levels is not necessary for inducing a decrease in erythrocyte velocity. Hyperglycemia is probably the main factor responsible for the decrease in microcirculatory flow in the BBD and WSTZ rats.

Animals↗

PubMed1976

Unsuspected diabetic glomerulosclerosis.

Six patients without overt diabetes mellitus underwent renal biopsy for suspected glomerulonephritis. All were demonstrated to have diabetic glomerulosclerosis and subsequently were found to have abnormal glucose tolerance tests. Electron microscopy was critical in making the correct diagnosis in five of six patients. The reported cases represent 3% of a series of 200 patients who had a renal biopsy to evaluate possible glomerulonephritis. Renal manifestations of diabetes mellitus may antedate glycosuria and other more common presenting symptoms of this disease.

Adult↗

PubMed1977

Chromium depletion in the pathogenesis of diabetes and atherosclerosis.

Dietary Cr deficiency may cause the aging-related Cr depletion observed in humans. Such depletion, when it occurs with excessive consumption of sugar and other carbohydrates, may result in glucose intolerance, glycosuria, hyperinsulinemia, and hyperlipidemia. These metabolic disorders could explain why athero-sclerotic diseases are endemic to most Western industrial societies. This review detailed significant current research and findings on the manifestations of Cr deficiency in humans and animal models.

Animals↗