scholarly journals Cold-induced dishabituation in rodents exposed to recurrent hypoglycaemia

Diabetologia ◽  
2021 ◽  
Author(s):  
Keeran Vickneson ◽  
Jessica Blackburn ◽  
Jennifer R. Gallagher ◽  
Mark L. Evans ◽  
Bastiaan E. de Galan ◽  
...  

Abstract Aims/hypothesis Recurrent hypoglycaemia in people with diabetes leads to progressive suppression of counterregulatory hormonal responses to subsequent hypoglycaemia. Recently it has been proposed that the mechanism underpinning this is a form of adaptive memory referred to as habituation. To test this hypothesis, we use two different durations of cold exposure to examine whether rodents exposed to recurrent hypoglycaemia exhibit two characteristic features of habituation, namely stimulus generalisation and dishabituation. Methods In the first study (stimulus generalisation study), hyperinsulinaemic–hypoglycaemic (2.8 mmol/l) glucose clamps were performed in non-diabetic rodents exposed to prior moderate-duration cold (4°C for 3 h) or control conditions. In the second study (dishabituation study), rodents exposed to prior recurrent hypoglycaemia or saline (154 mmol/l NaCl) injections over 4 weeks underwent a longer-duration cold (4°C for 4.5 h) exposure followed 24 h later by a hyperinsulinaemic–hypoglycaemic (2.8 mmol/l) glucose clamp. Output measures were counterregulatory hormone responses during experimental hypoglycaemia. Results Moderate-duration cold exposure blunted the adrenaline (epinephrine) response (15,266 ± 1920 vs 7981 ± 1258 pmol/l, Control vs Cold; p < 0.05) to next day hypoglycaemia in healthy non-diabetic rodents. In contrast, the suppressed adrenaline response (Control 5912 ± 1417 vs recurrent hypoglycaemia 1836 ± 736 pmol/l; p < 0.05) that is associated with recurrent hypoglycaemia was restored following longer-duration cold exposure (recurrent hypoglycaemia + Cold 4756 ± 826 pmol/l; not significant vs Control). Conclusions/interpretation Non-diabetic rodents exhibit two cardinal features of habituation, namely stimulus generalisation and dishabituation. These findings provide further support for the hypothesis that suppressed counterregulatory responses following exposure to recurrent hypoglycaemia in diabetes result from habituation. Graphical abstract

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 380 ◽  
Author(s):  
Utpal K. Prodhan ◽  
Shikha Pundir ◽  
Vic S.-C. Chiang ◽  
Amber M. Milan ◽  
Matthew P. G. Barnett ◽  
...  

Cooking changes the texture and tenderness of red meat, which may influence its digestibility, circulatory amino acids (AA) and gastrointestinal (GI) hormonal responses in consumers. In a randomised crossover intervention, healthy males (n = 12) consumed a beef steak sandwich, in which the beef was cooked by either a pan-fried (PF) or sous-vide (SV) method. Plasma AA were measured by ultrahigh performance liquid chromatography (UPLC), while plasma GI hormones were measured using a flow cytometric multiplex array. Following meat ingestion, the circulatory concentrations of some of the essential AA (all the branched-chain AA: leucine, isoleucine and valine; and threonine), some of the nonessential AA (glycine, alanine, tyrosine and proline) and some of the nonproteogenic AA (taurine, citrulline and ornithine) were increased from fasting levels by 120 or 180 min (p < 0.05). There were no differences in circulating AA concentrations between cooking methods. Likewise, of the measured GI hormones, glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) concentrations increased from fasting levels after consumption of the steak sandwich (p < 0.05), with no differences between the cooking methods. In the healthy male adults, protein digestion and circulating GI hormone responses to a beef-steak breakfast were unaltered by the different cooking methods.


Author(s):  
Flavio A. Cadegiani ◽  
Claudio E. Kater

Abstract Background Hormonal physiology in athletes, dysfunctional paths leading to overtraining syndrome (OTS), and clinical and biochemical behaviors that are independently modified by the presence of OTS remain unclear. Although multiple markers of OTS have recently been identified, the independent influence of OTS on hormones and metabolism have not been assessed. Hence, the objective of the present study was to uncover the previously unrecognized independent predictors of OTS and understand how OTS independently modifies the behaviors of clinical and biochemical parameters. Methods In a total of 39 athletes (OTS-affected athletes (OTS) = 14 and healthy athletes (ATL) = 25), we performed two clusters of statistical analyses using the full data of the Endocrine and Metabolic Responses on Overtraining Syndrome (EROS) study, in a total of 117 markers. We first used logistic regression to analyze five modifiable parameters (carbohydrate, protein, and overall caloric intake, sleep quality, and concurrent cognitive effort) as potential additional independent risk factors for OTS, and OTS as the outcome. We then used multivariate linear regression to analyze OTS as the independent variable and 38 dependent variables. Training patterns were found to be similar between OTS and ATL, and therefore excessive training was not a risk, and consequently not a predictor, for OTS. Results Each of the three dietary patterns (daily carbohydrate, daily protein, and daily overall calorie intake) were found to be the independent triggers of OTS, while sleeping, social, and training characteristics depended on other factors to induce OTS. Once triggered, OTS independently induced multiple changes, including reductions of cortisol, late growth hormone and adrenocorticotropic hormone responses to stimulations, testosterone-to-estradiol ratio, neutrophils, neutrophil-to-lymphocyte ratio, vigor levels, hydration status, and muscle mass, while increase of tension levels and visceral fat. Conclusions OTS can be independently triggered by eating patterns, regardless of training patterns, while the occurrence of OTS reduced late hormonal responses and the testosterone-to-estradiol ratio, worsened mood, and affected the immunology panel. These novel findings may explain underperformance, which is the key characteristic of OTS.


2006 ◽  
Vol 17 (3) ◽  
pp. 147
Author(s):  
Christopher C. Cheatham ◽  
Natalie Caine-Bish ◽  
Mark Blegen ◽  
Edward S. Potkanowicz ◽  
Gary H. Kamimori ◽  
...  

1999 ◽  
Vol 18 (6) ◽  
pp. 203-209 ◽  
Author(s):  
Olli Arjamaa ◽  
Lauri Turunen ◽  
Tero Malkinen ◽  
Jaana Laitinen ◽  
Juhani Leppaluoto ◽  
...  

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S130
Author(s):  
Christopher Cheatham ◽  
Natalie Caine-Bish ◽  
Mark Blegen ◽  
Edward S. Potkanowicz ◽  
Gary H. Kamimori ◽  
...  

1984 ◽  
Vol 247 (1) ◽  
pp. R114-R119
Author(s):  
J. Beard ◽  
W. Green ◽  
L. Miller ◽  
C. Finch

When exposed to an ambient temperature of 4 degrees C, iron-deficient anemic rats become hypothermic. This lesion is related more to anemia than to tissue iron deficiency, since exchange transfusion to hematocrits over 25 restored normal thermoregulatory performance. Likewise poor cold responses were induced in control rats by transfusion to low hematocrits. Cold sensitivity in all anemic animals was paralleled by poor thyroid responses: there was a significant positive correlation between hematocrit and percent rise in triiodothyronine (r = 0.63) and thyroxine (r = 0.53) during 6 h at 4 degrees C. Basal levels of thyroid-stimulating hormone (TSH) were similar in control and iron-deficient animals: after cold exposure, TSH rose to higher levels in those animals with hematocrits over 25 than in those with lower hematocrits. Diminished O2 delivery to tissues responsible for heat production is probably a major component of the cold sensitivity of anemic rats. The novel finding that thyroid hormone responses are compromised by anemia implies effects on hormonal regulation that may also contribute to this functional lesion.


1990 ◽  
Vol 37 (SUPPLEMENT) ◽  
pp. S45-S52 ◽  
Author(s):  
NORIAKI HARADA ◽  
MINORU NAKAMOTO ◽  
HIDEAKI KOHNO ◽  
HIROKAZU KONDO ◽  
MORISHIGE TANAKA

Author(s):  
Diogo V. Leal ◽  
Lee Taylor ◽  
John Hough

Purpose: Physical overexertion can lead to detrimental overreaching states without sufficient recovery, which may be identifiable by blunted exercise-induced cortisol and testosterone responses. A running test (RPETP) elicits reproducible plasma cortisol and testosterone elevations (in a healthy state) and may detect blunted hormonal responses in overreached athletes. This current study determined the salivary cortisol and testosterone responses reproducibility to the RPETP, to provide greater practical validity using saliva compared with the previously utilized blood sampling. Second, the relationship between the salivary and plasma responses was assessed. Methods: A total of 23 active, healthy males completed the RPETP on 3 occasions. Saliva (N = 23) and plasma (N = 13) were collected preexercise, postexercise, and 30 minutes postexercise. Results: Salivary cortisol did not elevate in any RPETP trial, and reduced concentrations occurred 30 minutes postexercise (P = .029, η2 = .287); trial differences were observed (P < .001, η2 = .463). The RPETP elevated (P < .001, η2 = .593) salivary testosterone with no effect of trial (P = .789, η2 = .022). Intraindividual variability was 25% in cortisol and 17% in testosterone. “Fair” intraclass coefficients of .46 (cortisol) and .40 (testosterone) were found. Salivary and plasma cortisol positively correlated (R = .581, P = .037) yet did not for testosterone (R = .345, P = .248). Conclusions: The reproducibility of salivary testosterone response to the RPETP is evident and supports its use as a potential tool, subject to further confirmatory work, to detect hormonal dysfunction during overreaching. Salivary cortisol responds inconsistently in a somewhat individualized manner to the RPETP.


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