Effects of fasting on blood plasma levels, metabolism and metabolic effects of epinephrine and norepinephrine in steers

1988 ◽  
Vol 118 (2) ◽  
pp. 254-259 ◽  
Author(s):  
Daniel Fröhli ◽  
Jürg W. Blum

Abstract. Experiments were designed to study effects of 3 days of fasting on blood plasma levels, metabolic clearance rates (MCR) and effects of norepinephrine (NE) and epinephrine (E) on levels of glucose, nonesterified fatty acids (NEFA) and immunoreactive insulin (IRI) in 12 steers. During fasting, levels of E, NE and protein did not change, whereas IRI, T3 and glucose decreased and NEFA, acetoacetate and β-hydroxybutyrate increased. Before and at the end of fasting, NE or E were iv infused for 120 min. NE and E were elevated after 15 min and to the end of the infusion. The increase in E, but not in NE, was significantly greater after 3 days of fasting than before fasting (P < 0.05). MCR for E was lower after fasting (299 ± 17 vs 204 ± 10 ml·kg−0.75·min−1; P < 0.001), whereas MCR for NE was not significantly different (455 ± 37 vs 400 ±27 ml·kg−0.75·min−1). MCR was higher for NE than for E, both before and after fasting (P < 0.05). After the infusions, E and NE decreased within minutes to pre-infusion concentrations. During E infusions, NEFA increased significantly more, whereas glucose increased less in fasted than in fed animals. During NE infusions, NEFA increased in fasted, but not in fed animals, and glucose increased less at the end than before fasting. IRI decreased during E infusions only in fed animals, and transiently increased after the infusion, except after NE infusion in fasted steers. Changes in plasma levels, clearance rates and sensitivity to effects of NE and E, together with alterations of insulin and T3 concentrations, may contribute to shifts in energy metabolism during food restriction.

1983 ◽  
Vol 97 (3) ◽  
pp. 327-338 ◽  
Author(s):  
W. J. de Greef ◽  
F. H. de Jong ◽  
J. de Koning ◽  
J. Steenbergen ◽  
P. D. M. van der Vaart

Steroid-free bovine follicular fluid (bFF) selectively suppresses the plasma levels of FSH in the female rat, demonstrating that bFF contains inhibin-like material. The present study was concerned with the effects of bFF on the hypothalamic release of LH releasing hormone (LH-RH) into hypophysial stalk blood and on the metabolic clearance rates of gonadotrophins. The metabolic clearance rates of FSH, LH and prolactin were determined after a single injection of and during a constant infusion with adenohypophysial extract. Similar results were obtained with both methods, and treatment with bFF did not alter the metabolic clearance rates of FSH, LH and prolactin. Anaesthesia with urethane, used for surgery involved in the collection of hypophysial stalk blood, did not interfere with the effect of bFF on plasma levels of FSH. The administration of bFF did not change the hypothalamic content of LH-RH, but caused a 30% decrease in the levels of LH-RH in hypophysial stalk plasma. However, a fraction isolated from bFF, which contained 20 times more inhibin-like activity per mg protein than bFF, did not alter the hypothalamic release of LH-RH into the hypophysial portal blood while this fraction was effective in specifically suppressing the plasma levels of FSH. It was concluded that the inhibin-like activity in bFF does not suppress the plasma levels of FSH by affecting its plasma clearance or by influencing the hypothalamic release of LH-RH, but that it has a direct effect on the adenohypophysis in inhibiting the release of FSH. Besides the inhibin-like activity, bFF also contains another factor which can decrease the levels of LH-RH in hypophysial stalk plasma.


2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Jose Rafael Villafan-Bernal ◽  
Mariana Acevedo-Alba ◽  
Rodrigo Reyes-Pavon ◽  
Guillermo Andres Diaz-Parra ◽  
Diana Lucia Lip-Sosa ◽  
...  

Background. Free fatty acids, also known as nonesterified fatty acids, are proinflammatory molecules that induce insulin resistance in nonpregnant individuals. Nevertheless, the concentration of these molecules has not been systematically addressed in pregnant women. Objective. This meta-analysis is aimed at evaluating the difference in free fatty acid plasma levels between women with gestational diabetes and healthy pregnant controls and their intrinsic and extrinsic determinants. Methods. We performed a systematic search to find relevant studies published in English and Spanish using PubMed, SCOPUS, and ISI Web of Knowledge. We included observational studies measuring the mean plasma levels of free fatty acids among gestational diabetes and healthy pregnant women, with at least ten subjects being analyzed in each group. The standardized mean difference (SMD) by random effects modeling was used. Heterogeneity was assessed using Cochran’s Q, H, and I2 statistics. Results. Among the 290 identified studies, twelve were selected for analysis. A total of 2426 women were included, from which 21% were diagnosed as having gestational diabetes. There were significantly higher levels of free fatty acids among women with gestational diabetes (SMD: 0.86; 0.54-1.18; p<0.001) when compared to healthy pregnant controls and between-study heterogeneity (I2=91%). The metaregression analysis showed that the gestational age at inclusion was the only cofactor influencing the mean levels of free fatty acids, indicating a trend towards lower plasma levels of free fatty acids later in gestation (estimate: -0.074; -0.143 to -0.004; p=0.036). No significant publication bias was found nor a trend towards greater results in small studies. Conclusions. Women with gestational diabetes have higher levels of free fatty acids when compared to healthy pregnant controls. More investigation is needed to assess the potential role of free fatty acids in the prediction of gestational diabetes earlier in pregnancy.


2007 ◽  
Vol 194 (2) ◽  
pp. 267-273 ◽  
Author(s):  
D C Ferguson ◽  
Z Caffall ◽  
M Hoenig

The obese cat is a model for the study of the progression toward type 2 diabetes. In this study, the impact of obesity on the hypothalamic–pituitary–thyroid axis was examined in 21 domestic shorthair cats before and after the development of obesity, which significantly increased body mass index (BMI), % body fat (BF), and girth (P<0.0001 for all). Serum total thyroxine (TT4), tri-iodothyronine, free T4 (FT4) by direct dialysis, nonesterified fatty acids (NEFA), and leptin were measured, and FT4 fraction (FFT4) was calculated. Serum thyrotropin (TSH) concentrations were measured in nine animals by validating a heterologous canine TSH assay with recombinant feline TSH as a standard. FT4, FFT4, NEFAs, and leptin were significantly higher in obese cats. FT4 had the strongest positive correlation with obesity indices BF, BMI, girth, NEFA, and leptin. Fatty acids oleate and palmitate were shown to inhibit T4 binding to pooled cat serum in vitro, suggesting the possibility that this mechanism was also relevant in vivo. Serum TT4 and TSH did not rise significantly. The implications for thyroid hormone (TH) action are not yet clear, but fatty acids have been proposed to inhibit the cellular uptake of TH and/or pituitary TH receptor binding, leading to TH resistance. Increased leptin may also alter sensitivity to negative feedback of TH. In conclusion, feline obesity is associated with a significant increase in FT4 within the normal range; future investigation into the cellular thyroid status will be necessary to establish cause and effect in this obesity model.


1975 ◽  
Vol 55 (4) ◽  
pp. 509-512 ◽  
Author(s):  
C. P. W. TSANG ◽  
A. J. HACKETT ◽  
E. M. TURNER Jr.

Estrone sulfate, estrone, and estradiol-17β have been assayed in blood plasma taken from the mammary vein of five pregnant cows before and after parturition. While there were considerable individual variations, the mean plasma levels of estrone sulfate (13.4 ng/ml), estrone (1 ng/ml) and estradiol-17β (1 ng/ml) remained fairly constant over the period of blood collection prior to parturition (−88 h to −2 h). The levels of all three estrogens dropped rapidly within 8 h postpartum. It is concluded that estrone sulfate, rather than estrone, is the predominant plasma estrogen in late pregnancy in the cow.


1957 ◽  
Vol 191 (2) ◽  
pp. 359-362 ◽  
Author(s):  
Edwin L. Bierman ◽  
Irving L. Schwartz ◽  
Vincent P. Dole

The mechanism by which carbohydrate utilization reduces the concentration of nonesterified fatty acids (NEFA) in plasma was studied by comparing the clearance of C14-labeled palmitic acid before and after the administration of insulin. The rate of disappearance from blood of a single injection of C14-labeled palmitic acid was identical before and after an intravenous injection of insulin (0.1 µ/kg) although the expected significant fall in total NEFA concentration occurred. When steady concentration of labeled NEFA was maintained by a constant infusion, the administration of insulin produced a significant increase in specific activity. It is, therefore, concluded that insulin decreases the release of fatty acids from tissue stores but does not accelerated their removal from blood.


1988 ◽  
Vol 255 (5) ◽  
pp. E668-E673 ◽  
Author(s):  
I. K. Martin ◽  
K. M. Weber ◽  
R. C. Boston ◽  
F. P. Alford ◽  
J. D. Best

Effects of four- to fivefold elevations of epinephrine (EPI) on glucose (Glc) metabolism were assessed in eight dogs before and after an intravenous Glc tolerance test, performed 30 min (short EPI) and 72 h (long EPI) after start of EPI infusion. Short EPI increased plasma nonesterified fatty acids (NEFA; 0.46 +/- 0.08 to 0.78 +/- 0.12 mmol/l, P less than 0.05), but Glc and insulin were unchanged. After long EPI, NEFA returned to control but Glc increased from 5.1 +/- 0.1 to 5.7 +/- 0.2 mmol/l (P less than 0.05). EPI reduced overall Glc tolerance (KG) from 3.5 +/- 0.7 to 2.5 +/- 0.2 (short EPI, P less than 0.05) and 2.3 +/- 0.3%/min (long EPI, P less than 0.02). Minimal model analysis showed that short EPI decreased insulin sensitivity (SI) from 7.9 +/- 1.1 to 4.2 +/- 1.2 min-1 per mU/l X 10(-4) (P less than 0.005) and increased pancreatic responsiveness (phi 1 from 3.7 +/- 0.3 to 7.4 +/- 2.9 mU/l.min-1 per mg/dl, P less than 0.025; phi 2 from 2.6 +/- 0.7 to 4.9 +/- 1.2 mU/l.min-2 per mg/dl). After long EPI SI, phi 1, and phi 2 returned to control. In contrast, Glc-mediated Glc disposal (SG) was decreased from 3.5 +/- 0.5 X 10(-2) to 2.8 +/- 0.6 X 10(-2) (short EPI) and 1.3 +/- 0.6 X 10(-2) min-1 (long EPI, P less than 0.02). We conclude that prolonged infusion of EPI leads to adaptation to its acute effects on NEFA, SI, phi 1, and phi 2.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 105 (9) ◽  
pp. e3316-e3328 ◽  
Author(s):  
Nantia Othonos ◽  
Thomas Marjot ◽  
Conor Woods ◽  
Jonathan M Hazlehurst ◽  
Nikolaos Nikolaou ◽  
...  

Abstract Context Glucocorticoids (GCs) are commonly prescribed, but their use is associated with adverse metabolic effects. 5α-reductase inhibitors (5α-RI) are also frequently prescribed, mainly to inhibit testosterone conversion to dihydrotestosterone. However, they also prevent the inactivation of GCs. Objective We hypothesized that 5α-RI may worsen the adverse effects of GCs. Design Prospective, randomized study. Patients A total of 19 healthy male volunteers (age 45 ± 2 years; body mass index 27.1 ± 0.7kg/m2). Interventions Participants underwent metabolic assessments; 2-step hyperinsulinemic, euglycemic clamp incorporating stable isotopes, adipose tissue microdialysis, and biopsy. Participants were then randomized to either prednisolone (10 mg daily) or prednisolone (10 mg daily) plus a 5α-RI (finasteride 5 mg daily or dutasteride 0.5 mg daily) for 7 days; metabolic assessments were then repeated. Main Outcome Measures Ra glucose, glucose utilization (M-value), glucose oxidation, and nonesterified fatty acids (NEFA) levels. Results Co-administration of prednisolone with a 5α-RI increased circulating prednisolone levels (482 ± 96 vs 761 ± 57 nmol/L, P = 0.029). Prednisolone alone did not alter Ra glucose (2.55 ± 0.34 vs 2.62 ± 0.19 mg/kg/minute, P = 0.86), M-value (3.2 ± 0.5 vs 2.7 ± 0.7 mg/kg/minute, P = 0.37), or glucose oxidation (0.042 ± 0.007 vs 0.040 ± 0.004 mmol/hr/kg/minute, P = 0.79). However, co-administration with a 5α-RI increased Ra glucose (2.67 ± 0.16 vs 3.05 ± 0.18 mg/kg/minute, P &lt; 0.05) and decreased M-value (4.0 ± 0.5 vs 2.6 ± 0.4 mg/kg/minute, P &lt; 0.05), and oxidation (0.043 ± 0.003 vs 0.036 ± 0.002 mmol/hr/kg, P &lt; 0.01). Similarly, prednisolone did not impair insulin-mediated suppression of circulating NEFA (43.1 ± 28.9 vs 36.8 ± 14.3 μmol/L, P = 0.81), unless co-administered with a 5α-RI (49.8 ± 8.6 vs 88.5 ± 13.5 μmol/L, P &lt; 0.01). Conclusions We have demonstrated that 5α-RIs exacerbate the adverse effects of prednisolone. This study has significant translational implications, including the need to consider GC dose adjustments, but also the necessity for increased vigilance for the development of adverse effects.


2004 ◽  
Vol 287 (3) ◽  
pp. E431-E438 ◽  
Author(s):  
Ramona Trebbien ◽  
Letty Klarskov ◽  
Mette Olesen ◽  
Jens J. Holst ◽  
Richard D. Carr ◽  
...  

Glucagon has a short plasma t1/2in vivo, with renal extraction playing a major role in its elimination. Glucagon is degraded by neutral endopeptidase (NEP) 24.11 in vitro, but the physiological relevance of NEP 24.11 in glucagon metabolism is unknown. Therefore, the influence of candoxatril, a selective NEP inhibitor, on plasma levels of endogenous and exogenous glucagon was examined in anesthetized pigs. Candoxatril increased endogenous glucagon concentrations, from 6.3 ± 2.5 to 20.7 ± 6.3 pmol/l [COOH-terminal (C)-RIA, P < 0.05]. During glucagon infusion, candoxatril increased the t1/2determined by C-RIA (from 3.0 ± 0.5 to 17.0 ± 2.5 min, P < 0.005) and midregion (M)-RIA (2.8 ± 0.5 to 17.0 ± 3.0 min, P < 0.01) and reduced metabolic clearance rates (MCR; 19.1 ± 3.2 to 9.4 ± 2.0 ml·kg−1·min−1, P < 0.02, C-RIA; 19.2 ± 4.8 to 9.0 ± 2.3 ml·kg−1·min−1, P < 0.05, M-RIA). However, neither t1/2nor MCR determined by NH2-terminal (N)-RIA were significantly affected ( t1/2, 2.7 ± 0.4 to 4.5 ± 1.6 min; MCR, 30.3 ± 6.4 to 28.5 ± 9.0 ml·kg−1·min−1), suggesting that candoxatril had no effect on NH2-terminal degradation but leads to the accumulation of NH2-terminally truncated forms of glucagon. Determination of arteriovenous glucagon concentration differences revealed that renal glucagon extraction was reduced (but not eliminated) by candoxatril (from 40.4 ± 3.8 to 18.6 ± 4.1%, P < 0.02, C-RIA; 29.2 ± 3.1 to 14.7 ± 2.2%, P < 0.02, M-RIA; 26.5 ± 4.0 to 19.7 ± 3.5%, P < 0.06, N-RIA). Femoral extraction was reduced by candoxatril when determined by C-RIA (from 22.7 ± 2.4 to 8.0 ± 5.1%, P < 0.05) but was not changed significantly when determined using M- or N-RIAs (10.0 ± 2.8 to 4.7 ± 3.7%, M-RIA; 10.5 ± 2.5 to 7.8 ± 4.2%, N-RIA). This study provides evidence that NEP 24.11 is an important mediator of the degradation of both endogenous and exogenous glucagon in vivo.


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