PROPOFOL AT SINGLE BOLUS AND CONTINUOUS RATE INFUSION SIGNIFICANTLY INCREASES SERUM TRIGLYCERIDES, BUT NOT CHOLESTEROL, IN HEALTHY BITCHES UNDERGOING ELECTIVE OVARIOHYSTERECTOMY

2021 ◽  
pp. 100560
Author(s):  
MA CHAGAS ◽  
LP CUSTODIO ◽  
BS GUSMÃO ◽  
IM COSTA ◽  
GH JULIÃO ◽  
...  
Keyword(s):  
Serum Triglycerides ◽  
Single Bolus ◽  
Rate Infusion

No Evidence for Short-Term Regulation of Plasminogen Activator Inhibitor Activity by Insulin in Man

1992 ◽  
Vol 67 (01) ◽  
pp. 117-120 ◽  
Author(s):  
Helena Vuorinen-Markkola ◽  
llpo Puhakainen ◽  
Hannele Yki-Järvinen
Keyword(s):  
Plasminogen Activator ◽  
Plasma Glucose ◽  
Serum Triglyceride ◽  
Plasminogen Activator Inhibitor ◽  
Saline Infusion ◽  
Serum Triglycerides ◽  
Serum Free ◽  
Free Insulin ◽  
Activator Inhibitor ◽  
Pai 1

SummaryIn crossectional studies a positive correlation has been found between circulating insulin, triglycerides and plasminogen activator inhibitor (PAI-1) activity. To directly examine the effect of insulin on PAI-1 activity in vivo, we determined the response of PAI-1 activity in 17 normal subjects to acute hyperinsulinemia (serum free insulin 92 ± 8 mU/l) during maintenance of normoglycemia (plasma glucose 5.1 ± 0.1 mmol/l). In 12 matched control subjects PAI-1 activity was measured during infusion of saline (serum free insulin 3.6 ± 0.3 mU/l, plasma glucose 5.2 ± 0.1 mmol/l). Plasma PAI-1 activity decreased during the insulin infusion from 9.0 α 1.4 to 5.6 α 0.8 U/ml (p <0.01), and during saline infusion from 7.0 ± 1.4 to 4.3 ± 0.6 U/ml (p <0.05). Serum triglyceride concentrations decreased from 1.09 ± 0.20 to 0.76 ± 0.09 mmol/l (p < 0.001) during hyperinsulinemia but remained unchanged during the saline infusion (1.04 ± 0.11 vs. 1.02 ± 0.12 mmol/l, NS). We conclude that insulin does not acutely change plasma PAI-1 activity, and that acute insulin-induced changes in serum triglycerides occur independently from those of PAI-1 activity.

Determinants of Plasminogen Activator Inhibitor-1 Activity in Survivors of Myocardial Infarction

1995 ◽  
Vol 73 (02) ◽  
pp. 261-267 ◽  
Author(s):  
Rosaire P Gray ◽  
Vidya Mohamed-Ali ◽  
David L H Patterson ◽  
John S Yudkin
Keyword(s):  
Myocardial Infarction ◽  
Plasminogen Activator ◽  
Plasma Insulin ◽  
Plasminogen Activator Inhibitor ◽  
Immunoreactive Insulin ◽  
Plasminogen Activator Inhibitor 1 ◽  
Serum Triglycerides ◽  
Fasting Plasma ◽  
Activator Inhibitor ◽  
Pai 1

SummaryA significant relationship has been described between plasminogen activator inhibitor-1 (PAI-1) and plasma insulin concentrations. However, most radioimmunoassays (RIA) substantially overestimate plasma insulin concentrations because of cross reaction with proinsulin-like molecules and it has been proposed that proinsulin-like molecules may be important determinants of PAI-1 activity. We measured fasting plasma immunoreactive insulin by conventional RIA, fasting plasma insulin (EIMA) by specific two site immuno-enzymometric assay, and intact proinsulin and des-31,32-proinsulin by two site immunoradiometric assay (IRMA) in 74 (50 nondiabetic and 24 diabetic) subjects who had survived a myocardial infarction between 6 and 24 months previously. In univariate analysis, PAI-1 activity correlated with serum triglycerides (rs=0.43; p <0.0001), insulin sensitivity (rs = -0.30; p = 0.004), and immunoreactive insulin (rs = 0.45; p <0.0001). However, the relationship between PAI-1 activity and plasma specific insulin (IEMA) was weaker (rs = 0.24; p = 0.019) than those with intact proinsulin (rs = 0.53; p <0.0001) and des-31,32-proinsulin (rs = 0.54; p <0.0001) despite the low concentrations of these proinsulin-like molecules. In multiple regression analysis, only des-31,32-proinsulin (p = 0.001) and serum triglycerides (p = 0.013) were significant determinants of PAI-1 activity. In conclusion, these results suggest that proinsulin-like molecules and serum triglycerides are important determinants of PAI-1 activity in survivors of myocardial infarction.

Counterregulation of insulin-induced hypoglycaemia in primary hypothyroidism

1986 ◽  
Vol 111 (4) ◽  
pp. 516-521
Author(s):  
Nina Clausen ◽  
Per-Eric Lins ◽  
Ulf Adamson ◽  
Bertil Hamberger ◽  
Suad Efendić
Keyword(s):  
Growth Hormone ◽  
Insulin Infusion ◽  
Primary Hypothyroidism ◽  
Constant Rate Infusion ◽  
Counterregulatory Hormones ◽  
Insulin Metabolism ◽  
Hormonal Responses ◽  
Glucose Levels ◽  
Constant Rate ◽  
Rate Infusion

Abstract. Hypothyroidism has been alleged to modulate insulin action and influence the secretion of growth hormone and catecholamines. We recently investigated the influence of hypothyroidism on glucose counterregulatory capacity and the hormonal responses to insulin-induced hypoglycaemia in 6 patients with primary hypothyroidism (age 32–52 years, TSH-values 66–200 mU/l). Hypoglycaemia was induced in the hypothyroid state and again when the subjects were euthyroid. After an overnight fast a constant rate infusion of insulin (2.4 U/h) was given for 4 h. Glucose was measured every 15 min and insulin, C-peptide, glucagon, epinephrine, norepinephrine, growth hormone and cortisol every 30 min for 5 h. During insulin infusion somewhat higher concentrations of the hormone were obtained in the hypothyroid state and simultaneously glucose levels were 0.5 mmol/l lower. As expected, basal norepinephrine levels were higher in hypothyroidism. However, no increase in circulating norepinephrine during hypoglycaemia was registered in the two experiments. The responses of counterregulatory hormones showed an enhanced response of cortisol, similar responses of growth hormone and epinephrine while the glucagon response was paradoxically impaired. Our findings suggest that hypothyroidism alters insulin metabolism, and that the glucagon response to hypoglycaemia is impaired in this condition.

Serum Lipid Profile in Diffuse versus Limited Systemic Sclerosis Data from the SASS cohort

2018 ◽  
Vol 69 (2) ◽  
pp. 403-406
Author(s):  
Codrina Ancuta ◽  
Cristina Pomirleanu ◽  
Cristina Iordache ◽  
Magda Ecaterina Antohe ◽  
Rodica Chirieac ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Lipid Profile ◽  
Total Cholesterol ◽  
Serum Lipid ◽  
Total Cholesterol Level ◽  
Cross Sectional Study ◽  
Serum Lipid Profile ◽  
Serum Triglycerides ◽  
Cross Sectional ◽  
Topoisomerase 1

Data about lipoprotein changes and their link with cardiovascular disease and atherosclerosis in systemic sclerosis (SSc) are still challenging. We aimed to evaluate serum lipid profile of patients with SSc and to identify potential relation with different disease specific characteristics (clinical, serological, inflammatory tests) in a cross-sectional study. Standard assessments comprised SSc-related parameters (disease subtype, clinical spectrum, immunological tests) and lipid metabolism (total cholesterol and fractions, triglycerides). Impaired lipid profile (low serum HDL- and high LDL-cholesterol, increased serum triglycerides, slightly modification in total cholesterol level) significantly correlated with diffuse SSc, activity (EUSTAR) and severity (MEDSGER), as well as seropositivity for specific antibodies (anti-centromere and anti-topoisomerase 1). The dyslipidemic profile might represent a pathobiological pathway for atherosclerosis in SSc.

The Effects of Coenzyme Q10 Supplementation on Lipid Profiles Among Patients with Metabolic Diseases: A Systematic Review and Meta-analysis of Randomized Controlled Trials

2018 ◽  
Vol 24 (23) ◽  
pp. 2729-2742 ◽  
Author(s):  
Nasrin Sharifi ◽  
Reza Tabrizi ◽  
Mahmood Moosazadeh ◽  
Naghmeh Mirhosseini ◽  
Kamran B. Lankarani ◽  
...  
Keyword(s):  
Systematic Review ◽  
Lipid Profile ◽  
Coenzyme Q10 ◽  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Meta Analysis ◽  
Lipid Profiles ◽  
Controlled Trials ◽  
Serum Triglycerides ◽  
Coq10 Supplementation

Background and objective: Oxidative stress and inflammation are key parameters in developing metabolic disorders. Hence, antioxidant intake might be an appropriate approach. Several studies have evaluated the effect of coenzyme Q10 (CoQ10) supplementation on lipid profile among patients with metabolic diseases, though findings are controversial. The aim of this systematic review and meta-analysis was to determine the effects of CoQ10 supplementation on lipid profile in patients with metabolic disorders. Methods: We searched PubMed, EMBASE, Web of Science and Cochrane Library databases until July 2017. Prospective clinical trials were selected assessing the effect of CoQ10 supplementation on different biomarkers. Two reviewers independently assessed the eligibility of studies, extracted data, and evaluated the risk of bias of included studies. A fixed- or random-effects model was used to pool the data, which expressed as a standardized mean difference with 95% confidence interval. Heterogeneity was measured using a Q-test and with I2 statistics. Results: A total of twenty-one controlled trials (514 patients and 525 controls) were included. The meta-analysis indicated a significant reduction in serum triglycerides levels (SMD -0.28; 95% CI, -0.56, -0.005). CoQ10 supplementation also decreased total-cholesterol (SMD -0.07; 95% CI, -0.45, 0.31), increased LDL- (SMD 0.04; 95% CI, -0.27, 0.36), and HDL-cholesterol levels (SMD 0.10; 95% CI, -0.32, 0.51), not statistically significant. Conclusion: CoQ10 supplementation may significantly reduce serum triglycerides levels, and help to improve lipid profiles in patients with metabolic disorders. Additional prospective studies are recommended using higher supplementation doses and longer intervention period.

Effect of muscular exercise on plasma viscosity in correlation with postprandial triglyceridemia

1963 ◽  
Vol 18 (5) ◽  
pp. 991-993 ◽  
Author(s):  
Aarne Konttinen ◽  
Timo Somer
Keyword(s):  
Triglyceride Level ◽  
Exercise Group ◽  
Plasma Viscosity ◽  
The Other ◽  
Muscular Exercise ◽  
Significant Elevation ◽  
Total Proteins ◽  
Serum Triglycerides ◽  
Lower Triglyceride Level ◽  
Fat Meal

The correlation between postprandial triglyceridemia and plasma viscosity was studied in 45 healthy young men. One-half, 23, of them carried out a heavy march lasting 2 hr while the other half, 22, rested in bed. Serum triglycerides and plasma viscosity were determined before the fat meal and 4 and 6 hr postprandially. Serum total proteins and hematocrits were measured simultaneously. Despite significantly higher postprandial triglyceridemia in the resting group no rise was seen in plasma viscosity, whereas, in the exercise group with a lower triglyceride level a significant elevation took place in plasma viscosity. serum triglycerides Submitted on February 18, 1963

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