scholarly journals Diabetes causes marked changes in function and metabolism of rat neutrophils

2006 ◽  
Vol 188 (2) ◽  
pp. 295-303 ◽  
Author(s):  
T C Alba-Loureiro ◽  
S M Hirabara ◽  
J R Mendonça ◽  
R Curi ◽  
T C Pithon-Curi
Keyword(s):  
Palmitic Acid ◽  
Citrate Synthase ◽  
Marked Change ◽  
Neutrophil Function ◽  
Diabetic Rats ◽  
Myristate Acetate ◽  
Diabetic State ◽  
High Incidence ◽  
And Function ◽  
Glucose 6 Phosphate Dehydrogenase

Several studies have shown impairment of neutrophil function, a disorder that contributes to the high incidence of infections in diabetes. Since glucose and glutamine play a key role in neutrophil function, we investigated their metabolism in neutrophils obtained from the peritoneal cavity of streptozotocin-induced diabetic rats. The activities of hexokinase, glucose-6-phosphate dehydrogenase (G6PDH), phosphofructokinase (PFK), citrate synthase, phosphate-dependent glutaminase, NAD+-linked and NADP+-linked isocitrate dehydrogenase were assayed. Glucose, glutamine, lactate, glutamate and aspartate, and the decarboxylation of [U-14C], [1-14C] and [6-14C]glucose; [U-14C]palmitic acid; and [U-14C]glutamine were measured in 1-h incubated neutrophils. Phagocytosis capacity and hydrogen peroxide (H2O2) production were also determined. All measurements were carried out in neutrophils from control, diabetic and insulin-treated (2–4IU/day) diabetic rats. Phagocytosis and phorbol myristate acetate (PMA)-stimulated H2O2 production were decreased in neutrophils from diabetic rats. The activities of G6PDH and glutaminase were decreased, whereas that of PFK was raised by the diabetic state. The activities of the remaining enzymes were not changed. Diabetes decreased the decarboxylation of [1-14C]glucose and [U-14C]glutamine; however, [6-14C]glucose and [U-14C]palmitic acid decarboxylation was increased. These observations indicate that changes in metabolism may play an important role in the impaired neutrophil function observed in diabetes. The treatment with insulin abolished the changes induced by the diabetic state even with no marked change in glycemia. Therefore, insulin may have a direct effect on neutrophil metabolism and function.

scholarly journals Diabetes causes marked changes in lymphocyte metabolism

2002 ◽  
Vol 174 (1) ◽  
pp. 55-61 ◽  
Author(s):  
R Otton ◽  
R Curi ◽  
Keyword(s):  
Lymph Nodes ◽  
Palmitic Acid ◽  
Citrate Synthase ◽  
Diabetic Rats ◽  
Lymphocyte Function ◽  
Mesenteric Lymph Nodes ◽  
Diabetic State ◽  
Mesenteric Lymph ◽  
Glucose 6 Phosphate Dehydrogenase

An enhanced susceptibility to infections is well known to occur in a poorly controlled diabetic state. Since glucose and glutamine are essential for lymphocyte function, we investigated whether their metabolism is changed in lymphocytes obtained from mesenteric lymph nodes of alloxan-induced diabetic rats (40 mg/kg body weight). The activities of hexokinase, phosphofructokinase, glucose-6-phosphate dehydrogenase (G6PDH), citrate synthase and phosphate-dependent glutaminase were determined. Decarboxylation of metabolites [U-14C]-, [1-14C]- and [6-14C]-glucose, [1-14C]- and [2-14C]-pyruvic acid, [U-14C]-palmitic acid and [U-14C]-glutamine was evaluated in incubated lymphocytes isolated from mesenteric lymph nodes. The measurements were carried out in cells following three experimental protocols: (1) lymphocytes freshly obtained from control and alloxan-induced diabetic rats, (2) lymphocytes from insulin-treated (2 U/rat per day) diabetic rats and (3) lymphocytes obtained from control and diabetic rats and cultured in the presence of insulin (1 mU/ml) for 6 h. The activities of hexokinase, G6PDH and citrate synthase were decreased by the diabetic state, whereas that of phosphofructokinase was raised. Decarboxylation of [U-14C]- and [6-14C]-glucose, [1-14C]- and [2-14C]-pyruvate and [U-14C]-glutamine were also decreased in lymphocytes from diabetic rats, whereas [U-14C]-palmitic acid decarboxylation was increased. Insulin administration in vivo or added to the culture medium reversed the changes observed in freshly obtained lymphocytes. Alloxan-induced diabetes did change lymphocyte metabolism and this may be an important mechanism leading to impairment of lymphocyte function.

Effects of insulin, glucocorticoids and thyroid hormones on the activities of key enzymes of glycolysis, glutaminolysis, the pentose-phosphate pathway and the Krebs cycle in rat macrophages

1992 ◽  
Vol 135 (2) ◽  
pp. 213-219 ◽  
Author(s):  
L. F. B. P. Costa Rosa ◽  
Y. Cury ◽  
R. Curi
Keyword(s):  
Thyroid Hormones ◽  
Pentose Phosphate Pathway ◽  
Culture Medium ◽  
Citrate Synthase ◽  
Inflammatory Responses ◽  
Krebs Cycle ◽  
Pentose Phosphate ◽  
Macrophage Phagocytosis ◽  
And Function ◽  
Glucose 6 Phosphate Dehydrogenase

ABSTRACT In the present study the effects of insulin, glucocorticoids and thyroid hormones on macrophage metabolism and function were investigated. The maximum activities of hexokinase, glucose-6-phosphate dehydrogenase, glutaminase and citrate synthase were determined in macrophages obtained from hormonetreated rats and those cultured for a period of 48 h in the presence of hormones. Macrophage phagocytosis was markedly inhibited by dexamethasone and thyroid hormones, remaining unchanged when insulin was added to the culture medium, however. The changes in the enzyme activities caused by hormone treatments of the rats were very similar to those found in culture. Insulin enhanced citrate synthase and hexokinase activities and diminished those of glutaminase and glucose-6-phosphate dehydrogenase. Dexamethasone had a similar effect except on glucose6-phosphate dehydrogenase. The addition of thyroid hormones to the culture medium raised the activities of glutaminase and hexokinase and reduced that of citrate synthase. The results presented support the suggestion that the effects of insulin, glucocorticoids and thyroid hormones on immune and inflammatory responses could well be mediated through changes in macrophage metabolism.. Journal of Endocrinology (1992) 135, 213–219

A PPARψ agonist improved diabetic state via decreasing TNF-α without any change including obesity in genetically obese diabetic rats

2001 ◽  
Vol 120 (5) ◽  
pp. A674-A674 ◽  
Author(s):  
A FUNAKOSHI ◽  
M ICHIKAWA ◽  
Y SATO ◽  
S KANAI ◽  
M OHTA ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Diabetic State ◽  
Tnf Α ◽  
Obese Diabetic Rats

Discordant effects of guanidines on renal structure and function and on regional vascular dysfunction and collagen changes in diabetic rats

Diabetes ◽  
1997 ◽  
Vol 46 (1) ◽  
pp. 94-106 ◽  
Author(s):  
J. R. Nyengaard ◽  
K. Chang ◽  
S. Berhorst ◽  
K. M. Reiser ◽  
J. R. Williamson ◽  
...  
Keyword(s):  
Vascular Dysfunction ◽  
Diabetic Rats ◽  
Structure And Function ◽  
Renal Structure ◽  
And Function

scholarly journals 145 President Oral Presentation Pick: Prenatal stress increases skeletal muscle mitochondrial volume density and function in yearling Brahman calves

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 120-121
Author(s):  
Chloey P Guy ◽  
Catherine L Wellman ◽  
David G Riley ◽  
Charles R Long ◽  
Ron D Randel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Prenatal Stress ◽  
Citrate Synthase ◽  
Volume Density ◽  
Assembly Factor ◽  
Mitochondrial Volume ◽  
Mitochondrial Volume Density ◽  
And Function

Abstract We previously determined that prenatal stress (PNS) differentially affected methylation of DNA from leukocytes of 28-d-old calves. Specifically, COX14 (cytochrome c oxidase (COX) assembly factor) and CKMT1B (mitochondrial creatine kinase U-type) were hypomethylated and COA5 (COX assembly factor 5), COX5A (COX subunit 5A), NRF1 (nuclear respiratory factor 1), and GSST1 (glutathione S-transferase theta-1) were hypermethylated in PNS compared to non-PNS calves (P ≤ 0.05). Our current objective was to test the hypothesis that PNS exhibit impaired mitochondrial function and greater oxidative stress than non-PNS calves. Blood and longissimus dorsi muscle samples were collected from yearling Brahman calves whose mothers were stressed by 2 h transportation at 60, 80, 100, 120, and 140 days of gestation (PNS; 8 bulls, 6 heifers) and non-PNS calves (4 bulls, 6 heifers). Serum was evaluated for the stress hormone, cortisol, and muscle damage marker, creatine kinase; muscle was analyzed for mitochondrial volume density and function by citrate synthase (CS) and COX activities, respectively, concentration of malondialdehyde, a lipid peroxidation marker, and activity of the antioxidant, superoxide dismutase (SOD). Data were analyzed using mixed linear models with treatment and sex as fixed effects. Serum cortisol was numerically higher in PNS than non-PNS calves but was not statistically different. Muscle CS and COX activities relative to protein were greater in PNS than non-PNS calves (P ≤ 0.03), but COX relative to CS activity was similar between groups. Activity of COX was greater in bulls than heifers (P = 0.03), but no other measure was affected by sex. All other measures were unaffected by PNS. Prenatal stress did not affect markers of muscle damage and oxidative stress in yearling Brahman calves at rest but mitochondrial volume density and function were greater in PNS calves. Acute stressors induce oxidative stress, so implications of differences in mitochondria in PNS calves following a stressor should be investigated.

Toll-like receptors stimulate human neutrophil function

Blood ◽  
2003 ◽  
Vol 102 (7) ◽  
pp. 2660-2669 ◽  
Author(s):  
Fumitaka Hayashi ◽  
Terry K. Means ◽  
Andrew D. Luster
Keyword(s):  
Immune Cell ◽  
Germ Line ◽  
Quantitative Polymerase Chain Reaction ◽  
Neutrophil Function ◽  
Human Neutrophils ◽  
Toll Like Receptors ◽  
Gm Csf ◽  
Latex Beads ◽  
Macrophage Colony ◽  
And Function

Abstract The first immune cell to arrive at the site of infection is the neutrophil. Upon arrival, neutrophils quickly initiate microbicidal functions, including the production of antimicrobial products and proinflammatory cytokines that serve to contain infection. This allows the acquired immune system enough time to generate sterilizing immunity and memory. Neutrophils detect the presence of a pathogen through germ line-encoded receptors that recognize microbe-associated molecular patterns. In vertebrates, the best characterized of these receptors are Toll-like receptors (TLRs). We have determined the expression and function of TLRs in freshly isolated human neutrophils. Neutrophils expressed TLR1, 2, 4, 5, 6, 7, 8, 9, and 10—all the TLRs except TLR3. Granulocyte-macrophage colony-stimulating factor (GM-CSF) treatment increased TLR2 and TLR9 expression levels. The agonists of all TLRs expressed in neutrophils triggered or primed cytokine release, superoxide generation, and L-selectin shedding, while inhibiting chemotaxis to interleukin-8 (IL-8) and increasing phagocytosis of opsonized latex beads. The response to the TLR9 agonist nonmethylated CpG-motif-containing DNA (CpG DNA) required GM-CSF pretreatment, which also enhanced the response to the other TLR agonists. Finally, using quantitative polymerase chain reaction (QPCR), we demonstrate a chemokine expression profile that suggests that TLR-stimulated neutrophils recruit innate, but not acquired, immune cells to sites of infection. (Blood. 2003;102:2660-2669)

scholarly journals Estrogen binding by leukocytes during phagocytosis,.

1977 ◽  
Vol 145 (4) ◽  
pp. 983-998 ◽  
Author(s):  
S J Klebanoff
Keyword(s):  
Chronic Granulomatous Disease ◽  
Reaction Mechanisms ◽  
Dehydrogenase Deficiency ◽  
Cell Types ◽  
Neutrophil Function ◽  
Granulomatous Disease ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Estrogen Binding ◽  
Two Populations

Estradiol binds covalently to normal leukocytes during phagocytosis. The binding involves three cell types, neutrophils, eosinophils, and monocytes and at least two reaction mechanisms, one involving the peroxidase of neutrophils and monocytes (myeloperoxidase [MPO]) and possibly the eosinophil peroxidase, and the second involving catalase. Binding is markedly reduced when leukocytes from patients with chronic granulomatous disease (CGD), severe leukocytic glucose 6-phosphate dehydrogenase deficiency, and familial lipochrome histiocytosis are employed and two populations of neutrophils, one which binds estradiol and one which does not, can be demonstrated in the blood of a CGD carrier. Leukocytes from patients with hereditary MPO deficiency also bind estradiol poorly although the defect is not as severe as in CGD. These findings are discussed in relation to the inactivation of estrogens during infection and the possible role of estrogens in neutrophil function.

REVASCULARIZATION AND FUNCTION OF PANCREATIC ISLET ISOGRAFTS IN DIABETIC RATS FOLLOWING TRANSPLANTATION.

2004 ◽  
Vol 78 ◽  
pp. 622-623
Author(s):  
H Furuya ◽  
T Kimura ◽  
M Morikawa ◽  
M Murakami ◽  
K Katayama ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Diabetic Rats ◽  
And Function
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