scholarly journals Circulating white blood cell count and measures of adipose tissue inflammation predict higher 24-h energy expenditure

2010 ◽  
Vol 162 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Jianying He ◽  
Duc Son Le ◽  
Xiaoyuan Xu ◽  
Michael Scalise ◽  
Anthony W Ferrante ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Blood Cell ◽  
Cell Count ◽  
Subclinical Inflammation ◽  
Blood Cell Count ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Pai 1

ObjectiveEnergy expenditure (EE) and measures of inflammation increase with adiposity, and this obesity-induced chronic and subclinical inflammation was extensively reported to be a cause of insulin resistance. However, whether subclinical inflammation has a role in increasing EE, which may be at the cost of developing insulin resistance, is not clear.MethodsWe investigated the association between circulating white blood cell count (WBC) in a population of Native Americans (n=243) with measurement of EE in a respiratory chamber, and in a subset of the same population (n=34), with gene expression measures of inflammation in subcutaneous abdominal adipose tissue (SAAT). All subjects were healthy on oral glucose tolerance test. Statistically, nonnormally distributed variables were logarithmically transformed before analyses to approximate normal distributions.ResultsWBC was associated with 24-h EE adjusted for age, sex, fat-free mass, and fat mass (r=0.13, P=0.04). In SAAT, tumor necrosis factor-α (TNF-α), shown as log10-transformed TNF-α (r=0.36, P=0.05), and plasminogen activator inhibitor-1 (PAI-1), shown as log10-transformed PAI-1 (lPAI-1; r=0.41, P=0.02), expressions were also positively correlated with adjusted 24-h EE. lPAI-1 was also correlated with adjusted sleep EE (r=0.34, P=0.07).ConclusionsIn conclusion, circulating markers of inflammation (WBC) and markers of inflammation within adipose tissue (TNF-α and PAI-1) are positively associated with EE, indicating a role of chronic subclinical inflammation in the regulation of metabolic rate.

Cigarette Smoking Increases Thromboxane A2 Formation without Affecting Platelet Survival in Young Healthy Females

1992 ◽  
Vol 68 (05) ◽  
pp. 583-588 ◽  
Author(s):  
Annika Dotevall ◽  
Christina Rångemark ◽  
Elsa Eriksson ◽  
Jack Kutti ◽  
Hans Wadenvik ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cigarette Smoking ◽  
Blood Cell ◽  
Urinary Excretion ◽  
Life Span ◽  
Cell Count ◽  
Thromboxane A2 ◽  
Blood Cell Count ◽  
Platelet Activity ◽  
Pai 1

SummarySmoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volunteers (aged 20–46 years, 18 smokers and 17 non-smokers) platelet life-span and indices of platelet activity were determined, together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen, peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p <0.05), while plasma and urinary β-thromboglobulin, plasma platelet factor 4, platelet mean life-span and platelet production rate did not differ between the groups. PAI-1 activity, white blood cell count and hematocrit were higher in smokers than in non-smokers (p <0.05). These data indicate that smoking facilitates platelet formation of thromboxane A2 without affecting platelet survival; i.e. it increases the activity of platelets without affecting their viability to a measurable extent. Such an increase in platelet activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit and white blood cell count, may play an etiological role in smoking-induced cardiovascular disease in women.

White blood cell count and insulin resistance in healthy nonsmoking men

1994 ◽  
Vol 127 (2) ◽  
pp. 459-461 ◽  
Author(s):  
Jorgen Lykke Jeppesen ◽  
Pierre Maheux ◽  
Francesco Stefano Facchini
Keyword(s):  
Insulin Resistance ◽  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Blood Cell Count

scholarly journals Effective Immunomodulatory Treatment of Escherichia coli Experimental Sepsis with Thalidomide

2003 ◽  
Vol 47 (8) ◽  
pp. 2445-2449 ◽  
Author(s):  
Evangelos J. Giamarellos-Bourboulis ◽  
Helen Poulaki ◽  
Nikolaos Kostomitsopoulos ◽  
Ismene Dontas ◽  
Despina Perrea ◽  
...  
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
White Blood Cell Count ◽  
White Blood Cell ◽  
Seed Oil ◽  
Experimental Sepsis ◽  
Bacterial Challenge ◽  
Blood Cell Count ◽  
Tnf Α ◽  
Vehicle Treated Control

ABSTRACT Thalidomide, an agent which inhibits biosynthesis of tumor necrosis factor alpha (TNF-α) and which is used to treat a variety of chronic inflammatory conditions, was investigated as therapy for experimental sepsis. Sepsis was induced by intraperitoneal injection of 107 CFU of Escherichia coli per kg of body weight to 80 Wistar rats divided into four groups. Group A consisted of 24 control animals that did not receive any pretreatment, group B consisted of 18 vehicle-treated control animals pretreated with seed oil, group C consisted of 30 rats administered thalidomide diluted in seed oil at a dose of 50 mg/kg 30 min before bacterial challenge, and group D consisted of eight animals that were not challenged with E. coli but that were used for white blood cell count determination. Sepsis was determined by measurement of vital signs before and 6 h after bacterial challenge. After 6 h the animals were killed and blood was sampled for culture; white blood cell count determination; and determination of endotoxin (lipopolysaccharide), TNF-α, interleukin-1β (IL-1β), and IL-6 levels. The levels of these cytokines were also estimated in the supernatants of human monocytes pretreated with thalidomide after exposure to the isolate. Sepsis developed in all vehicle-treated control animals and controls by 6 h after bacterial challenge but in only 10 animals (33.3%) pretreated with thalidomide (P < 0.0001). Six hours after bacterial challenge all animals had similar levels of endotoxemia, IL-1β, and IL-6. The mean white blood cell count for groups A, B, and C were 5,631.1, 2,638.9, and 8,169.3 cells/μl, respectively (P value between groups, <0.0001); the TNF-α levels were 77.3, 107.2, and 26.1 pg/ml, respectively (P values between groups, <0.0001). Pretreatment of human monocytes with thalidomide prevented the secretion of TNF-α and IL-1β but not that of IL-6. It is concluded that thalidomide exerts a considerable anti-inflammatory effect by preventing evolution to sepsis and by decreasing the level of production of TNF-α and therefore deserves to be further evaluated in research for the therapy of sepsis.

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