Modified colorimetric ultramicro method for estimating Nefa in serum

Elphick, Martin

doi:10.1136/jcp.21.5.567

Cited by 40 publications

(15 citation statements)

References 10 publications

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“…In Brazil, buffaloes between 100 and 200 days of lactation -submitted Serum contents for cholesterol, triglycerides, β-HBO and NEFA were quantified by enzymatic colorimetric methodology (WILLIAMSON; MALLANBY; KREBS, 1962;ELPHICK, 1968;ALLAIN et al, 1974;FOSSATI;PRENCIPE, 1982). The results for the first three were expressed in mmol L -1 , and for the last in µmol L -1 .…”

Section: Methodsmentioning

confidence: 99%

Lipid and glucose profiles of dairy buffaloes during lactation and dry period

Monteiro¹,

Yasuoka²,

Pogliani³

et al. 2012

RCA

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KEYWORDS Metabolism Lipids Serum Glucose Plasma PALAVRAS-CHAVE Metabolismo Lipídios Soro Glicose Plasma ABSTRACT:The purpose of this study was to analyze the influence of lactation and dry period in the constituents of lipid and glucose metabolism of buffaloes. One hundred fortyseven samples of serum and plasma were collected between November 2009 and July 2010, from properties raising Murrah, Mediterranean and crossbred buffaloes, located in the State of Sao Paulo, Brazil. Biochemical analysis was obtained by determining the contents of serum cholesterol, triglycerides, beta-hydroxybutyrate (β-HBO), non-esterified fatty acids (NEFA) and plasma glucose. Values for arithmetic mean and standard error mean were calculated using the SAS procedure, version 9.2. Tests for normality of residuals and homogeneity of variances were performed using the SAS Guide Data Analysis. Data were analyzed by ANOVA using the SAS procedure Glimmix. The group information (Lactation), Farm and Age were used in the statistical models. Means of groups were compared using Least Square Means (LSMeans) of SAS, where significant difference was observed at P ≤ 0.05. It was possible to conclude that buffaloes during peak lactation need to metabolize body reserves to supplement the lower amounts of bloodstream lipids, when they remain in negative energy balance. In the dry period, there were significant changes in the lipid profile, characterized by decrease of nutritional requirements, with consequent improvement in the general conditions of the animals. RESUMO: Com o objetivo de se analisar a influência da lactação e do período seco nos constituintes do metabolismo lipídico e na glicemia de búfalas leiteiras, foram coletadas amostras de soro e plasma de 147 animais, entre novembro de 2009 e julho de 2010, sendo estes oriundos de propriedades criadoras de búfalos das raças Murrah, Mediterrâneo e Mestiços, localizadas no Estado de São Paulo. A análise bioquímica foi obtida por meio da determinação dos teores séricos de colesterol, triglicérides, ß-hidroxibutirato (ß-HBO), ácidos graxos não esterificados (NEFA) e teores plasmáticos de glicose. Os valores da média aritmética e o erro padrão da média foram calculados utilizando-se o procedimento

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Section: Methodsmentioning

confidence: 99%

Lipid and glucose profiles of dairy buffaloes during lactation and dry period

Monteiro¹,

Yasuoka²,

Pogliani³

et al. 2012

RCA

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“…FFAs and leptin. Nonesterified FFA levels were measured using an enzymatic colorimetric assay (NEFA C test kit; Wako Chemicals, Richmond, VA) (44). FFA levels were measured at baseline and 30, 60, 90, 120, and 180 min into the euglycemic-hyperinsulinemic clamp procedure to assess sensitivity of FFAs to suppression by insulin.…”

Section: Methodsmentioning

confidence: 99%

Troglitazone Antagonizes Metabolic Effects of Glucocorticoids in Humans

et al. 2002

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Glucocorticoids induce insulin resistance in humans, whereas thiazolidinediones enhance insulin sensitivity. Although the effects of glucocorticoids and thiazolidinediones have been assessed in isolation, interaction between these drugs, which both act as ligands for nuclear receptors, has been less well studied. Therefore, we examined the metabolic effects of dexamethasone and troglitazone, alone and in combination, for the first time in humans. A total of 10 healthy individuals with normal glucose tolerance (age 40 ؎ 11 years, BMI 31 ؎ 6.1 kg/m 2) were sequentially studied at baseline, after 4 days of dexamethasone (4 mg/day), after 4 -6 weeks on troglitazone alone (400 mg/day), and again after 4 days of dexamethasone added to troglitazone. Key metabolic variables included glucose tolerance assessed by blood glucose and insulin responses to an oral glucose tolerance test (OGTT), insulin sensitivity evaluated via hyperinsulinemic-euglycemic clamp, free fatty acids (FFAs) and FFA suppressibility by insulin during the clamp study, and fasting serum leptin. Dexamethasone drastically impaired glucose tolerance, with fasting and 2-h OGTT insulin values increasing by 2.3-fold (P < 0.001) and 4.4-fold (P < 0.001) over baseline values, respectively. The glucocorticoid also induced a profound state of insulin resistance, with a 34% reduction in maximal glucose disposal rates (GDRs; P < 0.001). Troglitazone alone increased GDRs by 20% over baseline (P ‫؍‬ 0.007) and completely prevented the deleterious effects of dexamethasone on glucose tolerance and insulin sensitivity, as illustrated by a return of OGTT glucose and insulin values and maximal GDR to near-baseline levels. Insulin-mediated FFA suppressibility (FFA decline at 30 min during clamp/FFA at time 0) was also markedly reduced by dexamethasone (P ‫؍‬ 0.002). Troglitazone had no effect per se, but it was able to normalize FFA suppressibility in subjects coadministered dexamethasone. Futhermore, the magnitudes of response of FFA suppressibility and GDR to dexamethasone were proportionate. The same was true for the reversal of dexamethasone-induced insulin resistance by troglitazone, but not in response to troglitazone alone. Leptin levels were increased 2.2-fold above baseline by dexamethasone. Again, troglitazone had no effect per se but blocked the dexamethasone-induced increase in leptin. Subjects experienced a 1.7-kg weight gain while taking troglitazone but no other untoward effects. We conclude that in healthy humans, thiazolidinediones antagonize the action of dexamethasone with respect to multiple metabolic effects. Specifically, troglitazone reverses both glucocorticoid-induced insulin resistance and impairment of glucose tolerance, prevents dexamethasone from impairing the antilipolytic action of insulin, and blocks the increase in leptin levels induced by dexamethasone. Even though changes in FFA suppressibility were correlated with dexamethasone-induced insulin resistance and its reversal by troglitazone, a cause-and-effect relationship cannot be establ...

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“…Non-esterified fatty acids were quantified in duplicates as outlined by Elphick (1968) by using a kit (Wako Chemicals USA, Inc. Richmond, VA). Incubation was at 37°C for 5 min and absorbance was read at 550 nm.…”

Section: Non-esterified Fatty Acidsmentioning

confidence: 99%

Strong relationships between mediators of the acute phase response and fatty liver in dairy cows

Ametaj¹,

Bradford²,

Bobe³

et al. 2005

Can. J. Anim. Sci.

152

126

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. 2005. Strong relationships between mediators of the acute phase response and fatty liver in dairy cows. Can. J. Anim. Sci. 85: [165][166][167][168][169][170][171][172][173][174][175]. The objective of this study was to investigate the relationship between activation of acute phase response and fatty liver in transition dairy cows. Fatty liver was induced in dairy cows by feeding 8 kg of cracked corn 1 mo before the expected day of parturition. Liver and blood samples were obtained at days -4, 3, 8, 12, 14, 22, 27, and 36 postpartum. Cows that developed fatty liver (n = 4) reached peak total lipids in the liver at day 12 postpartum with 11.4% (wet wt.) compared with 6.6% in control cows (n = 4). Cows with fatty liver had greater plasma tumor necrosis factor-alpha (TNF-α), nonesterified fatty acids (NEFA), and lower lactate concentrations than did control cows at day -4. During highest concentrations of total lipids in the liver, for at least one time-point, fatty-liver cows had greater concentrations of plasma serum amyloid A (SAA), haptoglobin, and NEFA and lower concentrations of calcitonin gene-related peptide (CGRP), prostaglandin E 2 (PGE 2 ), cortisol, and TNF-α than did control cows. Concentrations of total lipids in the liver at 12 d postpartum were correlated (a) positively with plasma TNF-α, SAA, and NEFA and negatively with plasma CGRP before calving, (b) positively with plasma SAA, haptoglobin, and NEFA and negatively with plasma PGE 2 , CGRP, total cholesterol, and glucose at days 3, 8, and 12 postpartum, and (c) negatively with concentrations of plasma glucose, lactate, and total bilirubin after day 12 postpartum. In conclusion, this study indicates that the acute phase response occurs in cows with fatty liver as well as strong relationships between mediators of immune response and fatty liver. Mots clés: Réponse phase aiguë, foie gras, vaches laitièresFatty liver is a common metabolic disorder that affects almost half of all dairy cows immediately after parturition.Despite much progress in understanding metabolic events during the development of fatty liver, the precise mechanisms of the pathology remain unclear. The conventional view is that fatty liver is characterized by excess liver triacylglycerols (TAG) arising from a negative energy balance after parturition (Bauchart et al. 1998). The negative energy balance evokes a major mobilization of non-esterified fatty acids (NEFA) from adipose tissue and increased uptake of

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Modified colorimetric ultramicro method for estimating Nefa in serum

Cited by 40 publications

References 10 publications

Lipid and glucose profiles of dairy buffaloes during lactation and dry period

Lipid and glucose profiles of dairy buffaloes during lactation and dry period

Troglitazone Antagonizes Metabolic Effects of Glucocorticoids in Humans

Strong relationships between mediators of the acute phase response and fatty liver in dairy cows

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