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PubMed2005

Prospective evaluation of renal function in pediatric and adult patients treated with high-dose ifosfamide, cisplatin and high-dose methotrexate.

We investigated the renal function of pediatric and adult patients who had been submitted to chemotherapy with high-dose methotrexate (MTX), cisplatin and high-dose ifosfamide (IFO). We observed 43 osteosarcoma patients aged 4--34 years (median 16 years). The median received cumulative doses of MTX, cisplatin and IFO were 60.1 g/m, 598 mg/m and 73.5 g/m. Renal function was assessed by measurement of creatinine clearance, renal threshold for phosphate (Tmp/GFR), urinary alpha1-microglobulin (A1M):creatinine ratio, urinary albumin:creatinine ratio, 24-h glycosuria and proteinuria. The median interval between chemotherapy completion and first renal function assessment was 2 months (range 2--4 months); assessments were then performed at a median interval of 16 months (range 9--49 months). A significant decrease of TmP/GFR was observed only in the pediatric group (under 18 years): the percentage of patients with TmP/GFR<1 mmol/l increased from 21% (six of 28) at the end of treatment to 46% (13 of 28) at the late assessment. Glycosuria in 10 (67%) of 15 adults and 21 (75%) of pediatric patients was detected with an increased incidence compared to the early post-chemotherapy assessment (13% adults and 29% children). A significant increase of the albumin:creatinine ratio and A1M:creatinine ratio was observed only in adults. Overall, 21 patients had a reduced glomerular function at the latest evaluation, associated with glycosuria in 15 patients (71%), proteinuria in 14 (67%) and TmP/GFR<1 mmol/l in 11 (52%). We conclude that strict monitoring of renal function should be recommended in pediatric and adult patients after chemotherapy with high-dose MTX, cisplatin and high-dose IFO.

Acute Kidney Injury↗
PubMedDate not supplied

The quest for normoglycaemia: a historical perspective.

One of the longest-running controversies in medicine concerns the aims of diabetes treatment. The question debated for 80 years has been whether the clinician should just relieve symptoms, or try to achieve the much more difficult objective of near-physiological normality as measured by an absence of glycosuria and/or normal blood sugar levels. At the beginning of World War One, most clinicians and physiologists thought the severity of diabetes was inversely proportional to the number of functioning islets of Langerhans. Hyperglycaemia, it was hypothesized, stressed the surviving islets and led to a downward spiral of increasing glandular fatigue and hyperglycaemia. The aim of undernutrition was to rest the damaged tissue in the hope of promoting a return of functional efficiency and possibly regeneration. Most experts stressed that rest of the islets could only be achieved by abolishing glycosuria and restoring normal blood sugar levels. The first clinical use of insulin in 1922 led to astonishing improvements in the health and strength of patients with diabetes and the concept of pancreatic rest seemed to be confirmed when some regained such carbohydrate tolerance that after weeks or months they could reduce the dose of insulin without developing glycosuria. Initially there were expectations that insulin would allow the islets of Langerhans to recover completely, so that diabetes was cured. Most physicians insisted that the best chance of preserving what pancreatic function remained was biochemical normality. It was also contended that patients who had normal blood sugar levels were more healthy than those without and had fewer 'complications'. The complications in question were mainly infective, since specific diabetic tissue damage was not recognized until the late 1930s. The toll of microvascular complications (retinopathy and nephropathy) in those whose lives had been saved by insulin did not become apparent until the late 1930s and early 1940s, when it generated an often acrimonious debate about whether they were due to the metabolic disorder or an associated phenomenon. Liberalization of diet in patients taking insulin began in 1926 and by 1930 it was clear that patients who were prescribed 200 g of carbohydrate per day felt better and more energetic than those on the old regimens of 50 g or less per day. Even these more liberal diets were measured but, in the early 1930s some paediatricians, feeling that a strict measured diet was psychologically damaging, experimented with 'free' or unmeasured diets.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Glucose↗
PubMed1979

Effects of dietary cadmium on rhesus monkeys.

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.

Animals↗
PubMed1992

[Effect of sex hormones on the onset of diabetic syndrome in WBN/Kob rats].

The effects of sex hormone on diabetic conditions were investigated in WBN/Kob strain rats, i.e., castrated or spayed, hormone-treated, and non-treated rats. The effects of sex hormone on glycosuria, body-weight change, glucose tolerance and histopathology of the pancreas were compared among these animals. There were no abnormal changes in these parameters in the non-treated females and estrogen-treated males. The glycosuria began to be observed from the age of about 30 weeks in the non-treated group and from the age of 52 weeks in the castrated group. In the female animals, this symptom began to appear from the age of 55 weeks in the testosterone-treated group and from the age of 72 weeks in the spayed group. Before the onset of the diabetic symptoms, glucose tolerance was impaired in these animals. Body weights of the castrated and estrogen-treated males were lower than that of the non-treated males, especially in the estrogen-treated males. Those of the spayed and testosterone-treated females were much heavier than that of the non-treated females. Testosterone treatment accelerated body-weight gain in the spayed female animals. Histopathological examination of the pancreas revealed atrophy of the aciner tissue and atrophy and disappearance of the islet cells similar to those of the non-treated WBN/Kob male rats in the castrated males, spayed females and testosterone-treated females. However, these changes were not observed in the non-treated females or estrogen-treated males. These findings suggest that female hormone suppressed the onset of hyperglycemia along with glycosuria and male hormone accelerates the onset of hyperglycemia in the WBN/Kob rats.

Animals↗
PubMed1999

Calciotrophic hormones during experimental hypocalcaemia and hypercalcaemia in spontaneously diabetic rats.

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) concentrations have been found to be decreased in diabetic humans and rats. To investigate further the regulation of plasma Ca in diabetes, first we measured Ca(2+), P, Mg, parathyroid hormone(1-34) (PTH), and total and free 1,25(OH)(2)D(3) in male spontaneously diabetic rats 7 and 28 days after the onset of glycosuria. Secondly, we studied changes in the levels of PTH and 1,25(OH)(2)D(3) in response to hypocalcaemia induced by an i.v. infusion of EGTA (2.5%, wt/vol.) for 24 h, and changes in the levels of 1,25(OH)(2)D(3) in response to an i.v. infusion of rat PTH (10 microgram over 24 h) without or with concomitant EGTA infusion (producing hypercalcaemia or normo/hypocalcaemia respectively), in diabetic and control rats. Ca(2+), P, Mg and PTH concentrations remained within the control ranges after 7 and 28 days of glycosuria; 1,25(OH)(2)D(3) concentrations were decreased after 7, but not after 28, days of glycosuria. PTH concentrations showed a similar rise during EGTA-induced hypocalcaemia in control and diabetic rats compared with saline-infused rats, whereas 1,25(OH)(2)D(3) concentrations were unchanged in both groups. Total and free 1,25(OH)(2)D(3) levels were comparably (about 3-fold) increased during PTH, but not during combined PTH and EGTA infusion in control and diabetic rats. Total 1, 25(OH)(2)D(3) concentrations were lower in the diabetic groups infused with saline or PTH than in their respective controls, and there was a similar trend in the PTH+EGTA-infused group; free 1, 25(OH)(2)D(3) levels, however, were normal or increased in the diabetic groups, confirming our previous data. The novel finding of this study is that, despite severe insulin deficiency and altered 1, 25(OH)(2)D(3) levels, the in vivo response of PTH levels to hypocalcaemia and the in vivo response of 1,25(OH)(2)D(3) levels to PTH in diabetic rats are comparable with those found in nondiabetic rats.

Animals↗
PubMed1977

The spontaneously diabetic Wistar rat. Metabolic and morphologic studies.

A new, spontaneously diabetic syndrome has been recognized in nonobese outbred Wistar rats of both sexes. The age at detection of first glycosuria has varied from 48 to 120 days, with a mean of 67 days. Eighteen rats have been studied, 14 untreated and four during and after cessation of insulin treatment. The affected animals have demonstrated a spectrum of severity, with hyperglycemia (252-732 mg./dl.), hypoinsulinemia (0-1 ng./ml.), and hyperketonemia. The severely ketotic rats, with total blood ketone body levels between 6 and 13 mM, showed rapid loss in weight and dehydration over one to six days. The moderately ketotic (1-5 mM) declined gradually in weight over 15 days, with marked polyuria and glycosuria. The stable rats, with ketonemia less than 1 mM, sustained their weights, polyuria, and glycosuria for longer than 40 days. A relative or absolute increase in plasma immunoreactive glucagon and elevated levels of free fatty acids and branched-chain amino acids were observed in relation to the severity of the syndrome. Intraperitoneal arginine or tolbutamide elicited no insulin response, but the glucagon response to arginine was exaggerated. Pancreatic insulin content was normal or moderately decreased. Light-microscopic examination of pancreases of ketotic animals at the end stage of the disease showed islets to be very small and rare, consisting virtually of non-beta cells. In stable and earlier ketotic rats, the islets were small, with reduction in beta-cell number and a striking inflammatory cell infiltration. Surviving beta cells showed variable degranulation. This model of spontaneous diabetes in nonobese rats displays insulin deficiency, glucagon excess, and ketosis, with a dramatic inflammatory lesion during active beta-cell destruction.

Aging↗
PubMed2005

Point of care testing: a delight or a dilemma in the developing world?: an overview.

OBJECTIVES: This is to highlight the use of POCT especially by the untrained laboratorians, and its disadvantages and advantages. PATIENTS AND METHODS: The results of urinalysis carried out in Antenatal Clinic and Central Chemical Pathology laboratory for a two-year period were analysed to determine how the results were interpreted, whether there were further request(s) and how relevant they were. The results of 56 out of 303 oral glucose tolerance tests carried out because of positive glucose in urine (glycosuria) were reviewed. Similarly the results of 176 pregnant women who had proteinuria on urinalysis in Antenatal Clinic and 92 patients who had positive bilirubin-diglucuronide in their urine (bilirubinuria) were also reviewed. RESULTS: The result shows that only 18 out of the 56 patients who had OGTT based on positive glucose in their urine had glycosuria on fasting urine sample on the OGTT day. 4 of them had gestational diabetes mellitus, 2 were diabetic before conception 5 had impaired glucose tolerance, while 7 had renal glycosuria. Thirty-eight results were false positives with repeat urinalysis and OGTT. Also out of the 176 pregnant women who had proteinuria on urinalysis only 57(32.4%) were confirmed on repeat urinalysis and/or 24 hr urinary protein quantification, 51 became negative after successful treatment of their UTI, while 68(38.6%) were false positives. Similarly out of 92 patients who had bilirubinuria only 23 showed abnormalities suggestive of some degree of liver disease. CONCLUSION: Results obtained on POCT must be validated in the central laboratory.

Developing Countries↗
PubMed1994

Amelioration of diabetes and cataract by Na3VO4 plus U-83836E in streptozotocin treated rats.

Experimental work in our laboratory has confirmed the protective activity of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, diabetic cataract has also been partially prevented. Nevertheless, the combination of a natural antioxidant, vitamin E, with Na3 VO4 has not further enhanced this ameliorating effect. Our experimental approach has been an attempt to block the prooxidant activity of both STZ and vanadate, with the purpose of eliciting the best possible antidiabetic protection. More recently, a lipid soluble synthetic antioxidant U-78517F, a 2-methylaminochroman, has been reported to have a significant protective effect against brain injury and ischemia. This compound inhibits the iron-dependent lipid peroxidation 100 times more effectively than vitamin E. This investigation has introduced a combination of the vanadium compound plus the aforesaid lazaroid, as its (-) enantiomer, U-83836E, in order to improve the insufficient protection when vitamin E was used. For twelve weeks, male Wistar rats, rendered diabetic with STZ, were administered Na3VO4 in drinking water along with the lazaroid carried by the food. Four, eight and twelve weeks after the beginning of the protective treatment, fluid and food intake, diuresis and excreted feces, glycosuria and proteinuria were determined on biological samples obtained in metabolic cages; body weight and glycemia were also recorded. At weeks 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled and registered. At the end of the experiment, circulating glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG), and fluorescent peroxides were evaluated. Within the first month of treatment, protection by the combination paralleled that elicited by vanadate alone. At subsequent steps, U-83836E significantly improved the protective effect of vanadate alone on polydipsia and polyuria, but especially on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was also observed on HbA1c and NAG, and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered orally in food, in a non invasive manner.

Acetylglucosaminidase↗
PubMedDate not supplied

[Protective effect on nephropathy and on cataract in the streptozotocin-diabetic rat of the vanadium-lazaroid combination].

Experimental work from our laboratory has confirmed the protective power of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, the diabetic cataract too has been partially prevented. The protection slightly increased, when vanadium was administered in combination with vitamin E. This investigation has introduced a combination of Na3VO4 plus the lazaroid U-83836E, a liposoluble antioxidant much more efficacious than tocopherol, in order to improve the insufficient protection when vitamin E was used. Male Wistar rats, rendered diabetic with STZ, were treated for 12 weeks with Na3VO4 in drinking water, U-83836E carried by the food, or both. The most significant metabolic parameters (food and fluid intake, diuresis and excreted feces) were studied monthly by means of metabolic cages. Body weight, glycemia, glycosuria and proteinuria were also recorded. At week 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled. Circulation glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG) and fluorescent peroxides were evaluated at the end of the experiment. After the first month of treatment U-83836E improved significantly the protective effect of vanadate alone on polydipsia and polyuria, but more efficiently on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was observed also on HbA1c, NAG and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered per os, in a non invasive manner.

Animals↗
PubMedDate not supplied

[A prospective study on nephrotoxicity induced by continuous infusion of high-dose ifosfamide (15/m2)].

BACKGROUND: A good response rate to high-dose ifosfamide (HDIFO) has been reported in metastatic osteosarcoma and soft tissue tumors. As standard dose of IFO (< 12 g/m2) can give several renal complications and patients previously treated with nephrotoxic drugs are at high risk of nephrotoxicity, a prospective study to evaluate the pattern of nephrotoxicity induced by HDIFO was carried out. METHODS: Twelve patients (11 metastatic osteosarcoma, 1 synovial sarcoma; mean age 17, R 14-34) were treated with 4 courses of HDIFO/ MESNA (15 g/m2, IV 5 day continuous infusion with bicarbonate and K supplements). All but two were previously treated with cisplatin and methotrexate. Several parameters of renal function were measured before treatment, after each HDIFO course and two months after chemotherapy completion. RESULTS: Significant changes in the urinary excretion of beta 1-microglobulin, beta 2-microglobulin, Alanine Aminopeptidase, N-Acetil-beta, D-glucosaminidase and a significant reduction in phosphate tubular absorbtion according to the cumulative dose of IFO infused, were observed. Phosphaturia and hypophosphatemia occurred in all the patients studied. In 5 patients, CrCl fell below 70 ml/min with normal serum creatinine level after 45 g/m2 IFO. Plasma bicarbonate concentration less than 20 mmol/l was observed in 5 of 48 HDIFO courses. Glycosuria was detected in 4 patients. Two months after chemotherapy completion, mild glycosuria and slightly reduced CrCl persisted in two patients, whereas the other parameters of renal function studied were similar to the baseline values. An acute, usually reversible subclinical nephrotoxicity involving glomerule and renal tubule was demonstrated in all the patients treated with HDIFO. A persisting subclinical renal impairment was shown with mild glycosuria (2/12 patients) and slightly reduced CrCl (2/12 patients).

Adolescent↗
PubMed1982

Steroid diabetes in childhood.

Hyperglycemia and glycosuria are known to occur in some children receiving corticosteroids. In a retrospective study 24 such episodes were identified in 17 patients receiving steroids for a variety of primary diseases from 1968 to 1979. Detection based on symptoms averaged 26 days from initiation of steroid treatment, whereas detection based on the presence of glycosuria or hyperglycemia averaged 4.5 days. Acidosis, ketosis, and hyperglycemia (glucose level, greater than 500 mg/dL) occurred in 2, 4, and 8 patients, respectively. Insulin therapy was necessary in 15 episodes in 11 patients, but in three episodes the insulin dosage was reduced while the steroid dosage remained high. Permanent insulin dependence developed immediately in one patient and eventually in three others. Steroid-precipitated diabetes must be anticipated but should not interfere with the treatment of the primary disease.

Adolescent↗
PubMedDate not supplied

Phlorizin: a review.

The dihydrochalcone phlorizin is a natural product and dietary constituent found in a number of fruit trees. It has been used as a pharmaceutical and tool for physiology research for over 150 years. Phlorizin's principal pharmacological action is to produce renal glycosuria and block intestinal glucose absorption through inhibition of the sodium-glucose symporters located in the proximal renal tubule and mucosa of the small intestine. This review covers the role phlorizin has played in the history of diabetes mellitus and its use as an agent to understand fundamental concepts in renal physiology as well as summarizes the physiology of cellular glucose transport and the pathophysiology of renal glycosuria. It reviews the biology and pathobiology of glucose transporters and discusses the medical botany of phlorizin and the potential effects of plant flavonoids, such as phlorizin, on human metabolism. Lastly, it describes the clinical pharmacology and toxicology of phlorizin, including investigational uses of phlorizin and phlorizin analogs in the treatment of diabetes, obesity, and stress hyperglycemia.

Animals↗
PubMed2002

Association between renal dysfunction and mortality among inhabitants in the region around the Jinzu River basin polluted by cadmium.

A follow-up study was conducted on 5725 inhabitants (men 2858, women 2867) in and around the Jinzu River basin to determine the influence of environmental Cd exposure on mortality. In the Jinzu River basin, standardized mortality ratios (SMRs) investigated according to urinary findings (protein, glucose, and protein+glucose) were significantly low in the urinary protein-, glucose-, and protein+glucose-negative groups. SMRs calculated after dividing urinary protein- and glucose-positive status into two levels were lowest in the proteinuria- and glycosuria-negative groups and tended to be high in the higher positive groups. In the Jinzu River basin, Cox's hazard ratios were significantly higher for men and women in the urinary protein, glucose and protein+glucose-positive-groups. In the same analysis where the urinary protein- and glucose-positive subjects were divided into two levels, mortality was demonstrated to be higher in the groups with the greater degrees of proteinuria and glycosuria. In the Jinzu River water system almost all SMRs and Cox's hazard ratios showed statistical significance. This was not the case in the other water systems. Mortality of inhabitants with Cd-induced renal injury is increased in the Jinzu River basin.

Adult↗
PubMed1988

Alcohol consumption and impaired glycoregulation results in a population of 6665 salaried employees.

Alcohol consumption and glycosuria were found to be associated (p less than 0.001) in a population of 6571 salaried employees who underwent a systematic examination. The prevalence of glycosuria was found to range from 1.3% among 2609 non-drinkers to 5% among 816 heavy drinkers (six glasses or more of alcoholic beverage daily). This association was still significant after adjustment for age, sex and body mass index. Similarly, a positive association was observed between fasting glycemia and alcoholic intake in a subgroup of 998 subjects when such a result was available (p less than 0.05).

Adolescent↗
PubMed1975

The effect of phenformin-HCl on patients with diabetes mellitus, studied under strict balance conditions.

Under strict balance conditions we studied the effect of phenformin in 5 patients with diabetes mellitus. In all cases phenformin lowered the blood glucose values, and all patients showed a reduction of glycosuria. Contrary to other reports body weight increased during phenformin treatment. This was accompanied by positive nitrogen, phosphorus and calcium balances. The weight gain can be explained by the positive caloric balance, mainly caused by the diminished glycosuria. No change in B.M.R. or R.Q. was seen. During phenformin treatment there was a drop in cholesterol and total lipid levels in 4 patients. No conclusions could be drawn about the effect of phenformin on triglycerides, phospholipids and lipoprotein spectra. Phenformin treatment did not affect the disappearance of glucose, nor the insulin levels after intravenous glucose loading. During oral glucose loading phenformin caused a significant fall in blood glucose levels, accompanied by an increased insulin response in one patient. In the other 4 patients phenformin had no effect on either parameter.

Aged↗
PubMed1986

Chromium deficiency after long-term total parenteral nutrition.

A 63-year-old female developed unexplained hyperglycemia and glycosuria during administration of a total parenteral nutrition regimen on which she had been stable for several months. Because the patient had no history of diabetes or evidence of an infection, chromium deficiency was considered. Plasma chromium level was 0.1 microgram/dl (laboratory reference interval: 1.8-3.8 micrograms/dl). Fourteen days of supplemental intravenous chromium chloride (200 micrograms/day) allowed complete withdrawal of exogenous insulin with no further hyperglycemia or glycosuria. Correction of unexplained glucose intolerance following vigorous chromium supplementation indicates that the patient had chromium deficiency. Subsequent plasma chromium levels remained unchanged, possibly reflecting the sensitivity limits of the assay that was used, the uncertainty that exists regarding appropriate reference intervals for this element, and the fact that plasma levels do not always correlate with total body stores. The patient did not manifest peripheral neuropathy, which was present in one of the two previously reported cases, nor encephalopathy, which was reported in the other. We conclude that this patient developed chromium deficiency as a result of inadequate administration of chromium in the parenteral formula (6 micrograms/day) plus excessive enteric losses, and she presented with glucose intolerance as the only clinical manifestation of the deficiency. Caution should be exercised when interpreting plasma chromium in patients with suspected deficiency.

Blood Glucose↗
PubMed1984

Graded sucrose/carbohydrate diets in overtly hypertriglyceridemic diabetic patients.

Overtly hypertriglyceridemic patients with non-insulin-dependent diabetes mellitus were given a control diet containing 120 g of sucrose and 50 percent carbohydrate, and later randomly assigned to receive isocaloric high- (220 g), intermediate- (120 g), or low- (less than 3 g) sucrose/carbohydrate diets for four weeks. The low-sucrose diet group demonstrated a modest but significant decrease in mean fasting serum glucose level in the first week only, although this change was no different from the other two dietary groups and was not sustained. All groups had little change in late postprandial serum glucose levels from control values, and no significant alterations in 24-hour glycosuria. The high-sucrose diet group demonstrated a significant increase in fasting serum triglyceride levels by the second week of the study, whereas the intermediate- and low-sucrose diet groups showed a decrease in mean fasting triglyceride levels. In contrast, the low-sucrose diet group's late postprandial serum triglyceride levels increased by the fourth week, whereas levels fell in the high-sucrose diet group. Mean fasting serum cholesterol concentrations decreased from control values in the high-sucrose diet group. Thus, although very high sucrose and carbohydrate consumption is clearly deleterious to fasting tryglyceride levels in non-insulin-dependent diabetes mellitus with preexisting hypertriglyceridemia, it appears that low dietary sucrose and carbohydrate proportions do not further improve preprandial glycemia and glycosuria and may adversely affect late postprandial serum triglyceride concentration. This study suggests that isocaloric sucrose and carbohydrate restriction below usual daily levels (120 g per day) offers no consistent benefit in glycemia or lipid control in overt type II diabetes.

Blood Glucose↗
PubMed1987

Selected physical and biochemical parameters in the streptozotocin-treated guinea pig: insights into the diabetic guinea pig model.

Since evidence suggests that ascorbic acid deficits may provoke certain diabetic complications, it becomes necessary to develop a diabetic animal model which, like man, is unable to synthesize this vitamin. To this end, the present study monitored the diabetogenic effects of streptozotocin (STZ, 150 mg/kg) in the male guinea pig, a species rarely used in diabetes research. Over a 3-week period, body weight and relative food intake were lower in the STZ group compared to controls. The mean daily water intake and urine volume of the STZ group after 1 week were 175 and 270% of their initial pretreatment values, respectively, while control values were unchanged. The STZ group also exhibited a persistent glycosuria throughout the study. At the end of 3 weeks, aldehyde fuchsin staining of pancreatic beta cell granules (an index of stored insulin) was 58% lower in the STZ group compared to controls. Plasma C-peptide (indicator of insulin secretion) was expressed in human equivalents (mean +/- SEM). C-peptide was reduced in the STZ group (103 +/- 65 pg/ml) compared to controls (549 +/- 96 pg/ml); however, no change in plasma glucose was observed. Plasma ascorbic acid levels also were lower for STZ animals (150 +/- 26 micrograms%) versus controls (410 +/- 28 micrograms%). This study 1) demonstrates a diabetic syndrome in the STZ-treated guinea pig based on a reduced growth rate, beta cell dysfunction, polydipsia, polyuria and glycosuria, and 2) suggests the usefulness of this diabetic model in studies of pathologic mechanisms influenced by ascorbic acid.

Animals↗