Lactate is essential for maintenance of euglycemia in iron-deficient rats at rest and during exercise

1993 ◽  
Vol 264 (4) ◽  
pp. E662-E667 ◽  
Author(s):  
J. K. Linderman ◽  
P. R. Dallman ◽  
R. E. Rodriguez ◽  
G. A. Brooks
Keyword(s):  
Iron Deficiency ◽  
Hemoglobin Concentration ◽  
Liver Glycogen ◽  
Beta Blockade ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Iron Deficient ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Exercise Induced

To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.

Reciprocal changes of muscle oxidases and liver enzymes with recovery from iron deficiency

1989 ◽  
Vol 256 (3) ◽  
pp. E401-E405
Author(s):  
J. L. Azevedo ◽  
W. T. Willis ◽  
L. P. Turcotte ◽  
A. S. Rovner ◽  
P. R. Dallman ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Liver Enzymes ◽  
Hemoglobin Concentration ◽  
Glycolytic Enzyme ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Iron Administration ◽  
Sprague Dawley Rats ◽  
Iron Deficient ◽  
Time Courses

We determined the recovery time courses of muscle oxidases and liver enzymes after iron administration to iron-deficient rats. Female 21-day-old Sprague-Dawley rats were fed an iron-deficient (3 mg Fe/kg) or a control (50 mg Fe/kg) diet for 3 wk. The deficient rats were then injected with 50 mg Fe as iron dextran/kg body wt (Fe-T) or saline (Fe-) intraperitoneally. At 16, 40, 64, 112, and 180 h after injection, blood and tissue samples were taken to determine hemoglobin concentration (Hb), gastrocnemius glycolytic enzyme and oxidase activities, and liver amino acid catabolic enzyme activities. No changes were observed in any parameter across time in either the Fe- or control (Fe+) rats. In the Fe- rats, Hb, pyruvate + malate (P + M), 2-oxoglutarate (2-OG), and succinate oxidases (SO) were depressed to 33, 36, 44, and 7% of Fe+, respectively (P less than 0.05). At 16 h, Fe-T values were significantly elevated compared with Fe- rats but still only 40, 48, 55 and 10% of controls, respectively. Glutamate dehydrogenase (GDH) and alanine aminotransferase (AAT) of Fe- rats were 174 and 134% of control values (P less than 0.05). By the 180-h time point, Hb, P + M, 2-OG, and SO of Fe-T rats increased to 99, 84, 89, and 43% of Fe+ values, whereas GDH and AAT activities declined to 111 and 106% of controls. Glycolytic enzymes showed no systematic changes with iron deficiency or after iron administration.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Perturbed Vitamin A Status Induced by Iron Deficiency Is Corrected by Iron Repletion in Rats with Pre-Existing Iron Deficiency

2020 ◽  
Vol 150 (7) ◽  
pp. 1989-1995
Author(s):  
Yaqi Li ◽  
Cheng-Hsin Wei ◽  
Xia Xiao ◽  
Michael H Green ◽  
A Catharine Ross
Keyword(s):  
Iron Deficiency ◽  
Vitamin A ◽  
Kinetic Studies ◽  
Inhibitory Effect ◽  
Control Group ◽  
Sprague Dawley ◽  
Vitamin A Status ◽  
Sprague Dawley Rats ◽  
Iron Deficient ◽  
Plasma Retinol

ABSTRACT Background Although iron deficiency is known to interrupt vitamin A (VA) metabolism, the ability of iron repletion to restore VA metabolism and kinetics in iron-deficient rats is not well understood. Objectives In the present study, we examined the effects of dietary iron repletion on VA status in rats with pre-existing iron deficiency. Methods Weanling Sprague-Dawley rats were fed a VA-marginal diet (0.35 mg retinol/kg diet) containing either a normal concentration of iron [35 ppm, control group (CN)] or reduced iron (3 ppm, iron-deficient group, ID−); after 5 wk, 4 rats/group were killed for baseline measurements. A 3H-labeled retinol emulsion was administered intravenously to the remaining rats (n = 6, CN; n = 10, ID−) as tracer to initiate the kinetic study. On day 21 after dosing, n = 5 ID− rats were switched to the CN diet, generating an iron-repletion group (ID+). Blood samples were collected at 34 time points ≤92 d after dose administration, when all rats were killed and iron and VA status were determined. Results At baseline, ID− rats had developed iron deficiency, with a reduced plasma VA concentration (0.67 compared with 1.20 μmol/L in ID− and CN rats, respectively; P < 0.01) and a tendency toward higher liver VA (265 compared with 187 nmol in ID− and CN rats, respectively; P = 0.10). On day 92, iron deficiency persisted in ID− rats, accompanied by 2-times higher liver VA (456 nmol compared with 190 nmol in ID− and CN rats, respectively; P < 0.001) but lower plasma VA (0.64 compared with 0.94 μmol/L in ID− and CN rats, respectively; P = 0.05). ID+ rats not only recovered from iron deficiency, but also exhibited less liver VA sequestration (276 nmol) and normal plasma VA (0.91 μmol/L, not different from CN rats). Conclusions Our results suggest that iron repletion can remove the inhibitory effect of iron deficiency on hepatic mobilization of VA and restore plasma retinol concentrations in iron-deficient rats, setting the stage for kinetic studies of VA turnover in this setting.

Influence of autonomic blockade on cardiovascular responses to exercise in rats

1993 ◽  
Vol 75 (1) ◽  
pp. 155-161 ◽  
Author(s):  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Cardiovascular Responses ◽  
Beta Blockade ◽  
Sprague Dawley ◽  
Exercise Tests ◽  
Sprague Dawley Rats ◽  
Autonomic Blockade ◽  
Atropine Methyl Nitrate ◽  
Exercise Induced ◽  
Response To Exercise

The purposes of this study were to determine the role of the sympathetic and parasympathetic nervous systems in producing the heart rate (HR) response to dynamic exercise in rats and to determine the effect of attenuation of the HR response to exercise on blood flow redistribution. Sprague-Dawley rats (n = 10) were instrumented with arterial and venous catheters and Doppler flow probes. Mean arterial pressure (MAP), HR, mesenteric blood flow (MBF), and iliac blood flow (IBF) were determined during four exercise tests. On 4 consecutive days, rats were treated with saline (SAL, 1 mg/kg iv), atropine methyl nitrate (ATR, 2 mg/kg), timolol maleate (TIM, 0.5 mg/kg), and combined timolol and atropine. One minute of mild exercise (10 m/min) produced an increase in HR of 90 +/- 6 beats/min after SAL treatment, which was significantly less than the increment after ATR (56 +/- 5 beats/min) or TIM (4 +/- 3 beats/min). For the remainder of graded exercise, ATR treatment produced a modest attenuation in the increment in HR and no effect on MAP, IBF, and MBF. At 30 m/min, TIM markedly blunted the exercise-induced increment in HR (SAL, 138 +/- 8 beats/min; TIM, 53 +/- 4 beats/min) and IBF (SAL, 324 +/- 33%; TIM, 197 +/- 33%) with no effect on MAP or MBF. The results suggest that 1) the sympathetic nervous system is an important mediator of exercise-induced tachycardia in rats and 2) exercised-induced hyperemia, but not MAP, is attenuated by nonselective beta-blockade during exercise in rats.

scholarly journals Clinical thresholds for diagnosing iron deficiency: comparison of functional assessment of serum ferritin to population based centiles

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Gorkem Sezgin ◽  
Paul Monagle ◽  
Tze Ping Loh ◽  
Vera Ignjatovic ◽  
Monsurul Hoq ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Serum Ferritin ◽  
Age Groups ◽  
Hemoglobin Concentration ◽  
Population Based ◽  
Reference Intervals ◽  
Deficiency Anemia ◽  
Distribution Width ◽  
Iron Deficient ◽  
Lower Limits

Abstract Low serum ferritin is diagnostic of iron deficiency, yet its published lower cut-off values are highly variable, particularly for pediatric populations. Lower cut-off values are commonly reported as 2.5th percentiles, and is based on the variation of ferritin values in the population. Our objective was to determine whether a functional approach based on iron deficient erythropoiesis could provide a better alternative. Utilizing 64,443 ferritin test results from pediatric electronic health records, we conducted various statistical techniques to derive 2.5th percentiles, and also derived functional reference limits through the association between ferritin and erythrocyte parameters: hemoglobin, mean corpuscular volume, mean cell hemoglobin concentration, and red cell distribution width. We find that lower limits of reference intervals derived as centiles are too low for clinical interpretation. Functional limits indicate iron deficiency anemia starts to occur when ferritin levels reach 10 µg/L, and are largely similar between genders and age groups. In comparison, centiles (2.5%) presented with lower limits overall, with varying levels depending on age and gender. Functionally-derived limits better reflects the underlying physiology of a patient, and may provide a basis for deriving a threshold related to treatment of iron deficiency and any other biomarker with functional outcomes.

The Role of α-Thalassemia and Iron Deficiency in the Difference between Hemoglobin Levels of African-Americans (AA) and Whites.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3706-3706
Author(s):  
Ernest Beutler ◽  
Carol West
Keyword(s):  
Iron Deficiency ◽  
Serum Ferritin ◽  
Gene Frequency ◽  
Ferritin Level ◽  
Transferrin Saturation ◽  
Hemoglobin Concentration ◽  
Iron Deficient ◽  
High Prevalence ◽  
Hardy Weinberg Equilibrium ◽  
The Difference

Abstract The fact that the average hemoglobin concentration (Hb) of AA is lower than that of whites has been documented extensively. Several investigations have shown that this difference of approximately 0.8 g/dL is due neither to iron deficiency nor to socioeconomic status. Its cause remains unknown. We compared the Hb of 1,493 AA and 31,029 white anonymized patients attending a Health Appraisal Clinic and confirmed the known difference in Hb, both for females and males (0.79 and 0.47 g/dL) respectively. The difference persisted when a subset of the subjects were paired by age and narrowed slightly in females when those with serum ferritin levels of <10 ng/ml or transferrin saturations of <16% were excluded (difference in females 0.59 g/dL; males 0.47). We determined the α-thalassemia −3.7 genotype of 298 AA. The gene frequency was found to be 0.17, and the distribution of genotypes fit the Hardy-Weinberg equilibrium. However, in a sample of 155 white subjects only one α-thalassemia allele was found (gene frequency=0.003). Among the AA subjects, the Hb and MCV values were lower in homozygotes (−a/−a) and heterozygotes (aa/−a) for α-thalassemia than in the aa/aa subjects. The table presents data for AA and white subjects after excluding all who did not have a documented serum ferritin level of >9 ng/ml and a transferrin saturation of >16%. Excluding subjects with sickle trait had no effect. Ethnic Group Genotype n Mean Hb SE Hb Mean MCV SE MCV −a/−a 3 11.87 0.418 72.23 2.32 F AA aa/−a 20 12.69 0.202 85.22 0.86 aa/aa 65 13.17 0.127 90.43 0.61 White 2917 13.60 0.016 90.85 0.07 −a/−a 2 13.85 0.550 83.05 1.65 M AA aa/−a 36 14.37 0.161 85.81 0.78 aa/aa 86 14.75 0.123 89.78 0.53 White 5335 15.09 0.013 90.35 0.06 As shown in the table, the average Hb of non-iron deficient AA females and males who had 4 normal α loci (aa/aa) was 0.43 and 0.34 g/dL lower respectively than those of whites, the difference being significant with p<0.01. We conclude that one cause of the lower Hb of AA compared to white subjects is the high prevalence of α-thalassemia in the AA population, but that it accounts for only about one-quarter of the difference after iron deficiency has been excluded. There are other, as yet undefined, causes that play a role. These may include the lower ATP (Biochem. Genet.1:25, 1967) and higher 2,3 BPG (Transfusion18:108, 1978) levels that have been documented in the red cells of AA subjects.

scholarly journals Serum Natriuretic Peptides as Differential Biomarkers Allowing for the Distinction between Physiologic and Pathologic Left Ventricular Hypertrophy

2016 ◽  
Vol 45 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Michael E. Dunn ◽  
Thomas G. Manfredi ◽  
Kevin Agostinucci ◽  
Steven K. Engle ◽  
Josh Powe ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Left Ventricular ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Drug Induced ◽  
Peroxisome Proliferator Activated Receptor ◽  
Sprague Dawley Rats ◽  
Exercise Induced

Given the proven utility of natriuretic peptides as serum biomarkers of cardiovascular maladaptation and dysfunction in humans and the high cross-species sequence conservation of atrial natriuretic peptides, natriuretic peptides have the potential to serve as translational biomarkers for the identification of cardiotoxic compounds during multiple phases of drug development. This work evaluated and compared the response of N-terminal proatrial natriuretic peptide (NT-proANP) and N-terminal probrain natriuretic peptide (NT-proBNP) in rats during exercise-induced and drug-induced increases in cardiac mass after chronic swimming or daily oral dosing with a peroxisome proliferator-activated receptor γ agonist. Male Sprague-Dawley rats aged 8 to 10 weeks were assigned to control, active control, swimming, or drug-induced cardiac hypertrophy groups. While the relative heart weights from both the swimming and drug-induced cardiac hypertrophy groups were increased 15% after 28 days of dosing, the serum NT-proANP and NT-proBNP values were only increased in association with cardiac hypertrophy caused by compound administration. Serum natriuretic peptide concentrations did not change in response to adaptive physiologic cardiac hypertrophy induced by a 28-day swimming protocol. These data support the use of natriuretic peptides as fluid biomarkers for the distinction between physiological and drug-induced cardiac hypertrophy.

scholarly journals Effect of Maternal Iron Deficiency Anemia on the Iron Store of Newborns in Ethiopia

Anemia ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Betelihem Terefe ◽  
Asaye Birhanu ◽  
Paulos Nigussie ◽  
Aster Tsegaye
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Serum Ferritin ◽  
Complete Blood Count ◽  
Iron Status ◽  
Hemoglobin Concentration ◽  
Deficiency Anemia ◽  
Iron Store ◽  
Cross Sectional ◽  
Iron Deficient

Iron deficiency anemia among pregnant women is a widespread problem in developing countries including Ethiopia, though its influence on neonatal iron status was inconsistently reported in literature. This cross-sectional study was conducted to compare hematologic profiles and iron status of newborns from mothers with different anemia status and determine correlation between maternal and neonatal hematologic profiles and iron status in Ethiopian context. We included 89 mothers and their respective newborns and performed complete blood count and assessed serum ferritin and C-reactive protein levels from blood samples collected from study participants. Maternal median hemoglobin and serum ferritin levels were 12.2 g/dL and 47.0 ng/mL, respectively. The median hemoglobin and serum ferritin levels for the newborns were 16.2 g/dL and 187.6 ng/mL, respectively. The mothers were classified into two groups based on hemoglobin and serum ferritin levels as iron deficient anemic (IDA) and nonanemic (NA) and newborns of IDA mothers had significantly lower levels of serum ferritin (P=0.017) and hemoglobin concentration (P=0.024). Besides, newborns’ ferritin and hemoglobin levels showed significant correlation with maternal hemoglobin (P=0.018;P=0.039) and ferritin (P=0.000;P=0.008) levels. We concluded that maternal IDA may have an effect on the iron stores of newborns.

Reversibility of exercise-induced dendritic attenuation in brain cardiorespiratory and locomotor areas following exercise detraining

2006 ◽  
Vol 101 (4) ◽  
pp. 1243-1251 ◽  
Author(s):  
Amanda J. Nelson ◽  
Gary A. Iwamoto
Keyword(s):  
Heart Weight ◽  
Sprague Dawley ◽  
Hypothalamic Area ◽  
Sprague Dawley Rats ◽  
Cuneiform Nucleus ◽  
Dendritic Branching ◽  
The Mean ◽  
Exercise Induced ◽  
Ring Analysis ◽  
The Brain

It has been shown previously that dendritic branching in cardiorespiratory and locomotor brain areas can be attenuated with exercise training (ET). It was not known whether this process was reversible. Twenty-three ( n = 23) male Sprague-Dawley rats were individually caged and divided into two groups: untrained (UN; n = 11) and detrained (DTR; n = 12). DTR were provided with a running wheel at 21 days of age and exercised spontaneously. After 120 days (70 days of ET followed by 50 days of detraining), ET indexes were obtained, including maximal oxygen uptake, percent body fat, resting heart rate, and heart weight-to-body weight ratios. The brain was processed according to a modified Golgi-Cox procedure. Impregnated neurons from the periaqueductal gray (PAG), posterior hypothalamic area (PH), nucleus of the tractus solitarius (NTS), and cuneiform nucleus (CfN) were examined in coronal sections. Neurons were traced using a camera lucida technique and analyzed using the Sholl concentric ring analysis of dendritic branching. t-Tests compared the mean number of intersections per neuron by grouping inner rings, outer rings, and total number of intersections per animal. There were no significant differences between UN and DTR in PH, PAG, CfN, and NTS in the inner rings, outer rings, and total number of intersections per animal. A separate group of animals was used to show that a training effect in the CfN and NTS was present at 56 days of ET. Our results show that dendritic attenuation resulting from 70 days of ET in PH, PAG, CfN, and NTS is completely reversed with 50 days of detraining.

Effect of adrenodemedullation on decline in muscle malonyl-CoA during exercise

1993 ◽  
Vol 74 (5) ◽  
pp. 2548-2551 ◽  
Author(s):  
W. W. Winder ◽  
R. W. Braiden ◽  
D. C. Cartmill ◽  
C. A. Hutber ◽  
J. P. Jones
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Malonyl Coa ◽  
Exercise Induced ◽  
Rate Limiting

Malonyl-CoA is an inhibitor of carnitine palmitoyltransferase, a rate-limiting enzyme of fatty acid oxidation. Previous studies have indicated that muscle malonyl-CoA declines in rats during treadmill running. This decrease may be important for allowing an increased rate of fatty acid oxidation during prolonged exercise. This study was designed to determine whether epinephrine is essential for inducing the decline in muscle malonyl-CoA during exercise. Male Sprague-Dawley rats underwent adrenodemedullation (ADM) or sham operation. After allowing 3 wk for recovery, rats were killed (pentobarbital anesthesia) at rest or after running at 21 m/min up a 15% grade for 60 min. Red quadriceps malonyl-CoA decreased from 2.6 +/- 0.3 to 0.8 +/- 0.07 nmol/g in sham-operated rats and from 2.2 +/- 0.3 to 0.8 +/- 0.1 nmol/g in ADM rats. White quadriceps malonyl-CoA decreased to similar levels during exercise in both sham-operated and ADM rats. A second experiment on 24-h fasted rats also showed no impairment in the exercise-induced decline in red quadriceps malonyl-CoA as a result of adrenodemedullation. The hormones of the adrenal medulla are therefore unessential for inducing the decline in malonyl-CoA during exercise.

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