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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary iron deficiency in rats results in increased blood glucose turnover and recycling. We measured the rates of glucose production in isolated hepatocytes from iron-sufficient (Fe+) and iron-deficient (Fe-) rats to assess the intrinsic capacity of the Fe- liver to carry out gluconeogenesis. Low-iron and control diets were given to 21-day-old female rats. After 4-5 wk, hemoglobin concentrations averaged 4.1 g/dl in the Fe- and 14.3 g/dl in the Fe+ animals. In the hepatocytes from Fe- rats, there was a 35% decrease in the rate of glucose production from 1 mM pyruvate + 10 mM lactate, a 48% decrease from 0.1 mM pyruvate + 1 mM lactate, a 39% decrease from 1 mM alanine, and a 48% decrease from 1 mM glycerol. The addition of 5 microM norepinephrine or 0.5 microM glucagon to the incubation media produced stimulatory effects on hepatocytes from both Fe- and Fe+ rats, resulting in the maintenance of an average difference of 38% in the rates of gluconeogenesis between the two groups. Studies on isolated liver mitochondria and cytosol revealed alpha-glycerophosphate-cytochrome c reductase and phospho(enol)pyruvate carboxykinase activities to be decreased by 27% in Fe- rats. We conclude that because severe dietary iron deficiency decreases gluconeogenesis in isolated rat hepatocytes, the increased gluconeogenesis demonstrated by Fe- rats in vivo is attributable to increased availability of gluconeogenic substrates and upregulation of the pathway.
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PMID:Iron deficiency decreases gluconeogenesis in isolated rat hepatocytes. 260 20

The effect of sucrose overfeeding and low iron diet on brown adipose tissue (BAT) thermogenesis of rats has been investigated from the view point of in vitro BAT oxygen consumption and BAT fatty acids (FA) compositions in rats. Control group was fed on a standard diet with tap water, sucrose group was on the standard diet and 32% sucrose solution, and iron deficient group on a low iron diet with tap water. In vitro interscapular BAT thermogenesis as estimated by oxygen consumption was measured in minced tissue blocks in Krebs-Ringer phosphate buffer using a Clark oxygen electrode. In sucrose overfeeding rats, caloric intake was greater than in controls, but did not differ body weight. Interscapular BAT weight and DNA content were greater. Colonic and tail skin temperatures were higher. Basal oxygen consumption was higher. Noradrenaline- and glucagon-stimulated oxygen consumptions did not differ when expressed per DNA, but significantly greater per whole tissue pad. Both BAT-triglyceride (TG) and -phospholipid (PL) levels were higher. Polyunsaturated FA were lower, while monosaturated FA were higher in both BAT-TG and -PL. In iron deficient rats, BAT weight and DNA content were higher. Colonic and tail skin temperatures did not differ. Although basal oxygen consumption did not differ, noradrenaline-stimulated oxygen consumption was less per DNA, but did not differ per whole tissue pad, while glucagon-stimulated oxygen consumption was less when expressed per DNA, as well as whole tissue pad. Cold-tolerance as assessed by the fall in colonic temperature at 0 degree C was decreased. BAT-TG and -PL levels did not differ. Polyunsaturated FA were higher in both BAT-TG and -PL. These findings indicated that sucrose-induced overfeeding enhances BAT thermogenesis mainly by tissue hyperplasia, while iron deficiency suppresses BAT thermogenic response, although it causes the compensatory tissue hyperplasia.
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PMID:[Nutritional adaptation in brown adipose tissue thermogenesis--with special reference to overfeeding and iron deficiency]. 786 52

To evaluate the hypothesis that mild iron deficiency increases dependence upon gluconeogenesis, control and mildly iron-deficient (Hb = 80 +/- 2 g/L) rats were injected with mercaptopicolinic acid (MPA), a known inhibitor of gluconeogenesis, or with injection vehicle (sham) and studied at rest or after 30 min of treadmill running (13.4 m/min, 0% grade). Liver glycogen concentration was lower in resting iron-deficient rats than in resting control rats, but iron deficiency did not influence arterial substrates or hormones in sham-treated rats. Glucose and insulin concentrations were less in resting control and iron-deficient MPA-treated rats than in sham-treated animals. However, arterial lactate was greater in resting iron-deficient MPA-treated rats than control MPA-treated animals, and glucagon and epinephrine were greater in resting iron-deficient MPA-treated rats than in iron-deficient sham-treated animals, indicating that gluconeogenesis is more important to maintenance of euglycemia in resting iron-deficient animals than in controls. Moderate exercise stimulated glucose metabolism in iron-deficient rats, as evidenced by the lower arterial glucose and higher arterial lactate when compared with resting iron-deficient rats. However, MPA treatment did not clearly establish differences between iron-deficient and control rats after exercise. Therefore, changes in substrate and hormone concentrations in resting iron-deficient MPA-treated rats indicate that dependence on gluconeogenesis for maintenance of euglycemia is greater at rest with dietary iron deficiency. Furthermore, consistent with previously published results for severely iron-deficient rats, results from the present investigation indicate that dependence on glucose metabolism is greater during moderate exercise in mildly iron-deficient rats.
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PMID:Maintenance of euglycemia is impaired in gluconeogenesis-inhibited iron-deficient rats at rest and during exercise. 796 96

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.
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PMID:Lactate is essential for maintenance of euglycemia in iron-deficient rats at rest and during exercise. 809 76

We hypothesized that augmented responses of glucoregulatory hormones in iron deficiency would enhance liver and muscle glycogenolysis, leading to increased gluconeogenic precursor (lactate) supply and upregulation of hepatic gluconeogenesis. Female weanling rats were randomly placed on either a mildly iron-deficient (-Fe; 15 mg Fe/kg diet) or an iron-sufficient (+Fe; 50 mg Fe/kg diet) diet for 4 wk and studied at rest and during exhaustive treadmill running. Hemoglobin was 9.0 +/- 0.2 and 13.1 +/- 0.3 g/dl in -Fe and +Fe, respectively, after 3.5 wk of dietary iron deficiency. Arterial plasma epinephrine (Epi), norepinephrine (NE), adrenocorticotropic hormone (ACTH), corticosterone, insulin, and glucagon levels were similar at rest in both groups, as were liver, gastrocnemius, and superficial and deep vastus medialis glycogen levels. Liver and kidney phosphoenolpyruvate carboxykinase (PEPCK) activities were similar in both groups. Maximum O2 consumption was decreased (22%) in -Fe. Respiratory exchange ratio (CO2 production/O2 consumption) was unaffected at rest but increased at maximum O2 consumption in -Fe. Time to exhaustion during a standardized running test (13.4 m/min, 0% grade) was decreased 45% in -Fe (63 +/- 5 vs. 116 +/- 10 min). During exercise, euglycemia was maintained in both groups, but blood lactate was elevated in -Fe. The mean net glycogen utilization during exercise was increased in liver (43%), soleus (33%), and superficial vastus medialis (106%) and decreased in the gastrocnemius (36%) in -Fe. Liver and kidney PEPCK activities were increased similarly at exhaustion in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented glucoregulatory hormone concentrations during exhausting exercise in mildly iron-deficient rats. 823 58