Noradrenaline-induced secretions of pancreatic hormones in cold- and heat-acclimated rats.

Kuroshima, Akihiro; Habara, Yoshiaki; Ohno, Tomie

doi:10.2170/jjphysiol.33.827

Cited by 5 publications

(3 citation statements)

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“…The present result clearly indicated that cold acclimation causes a potentiation in glucagon-secreting action of noradrenaline, confirming the previous study that NA infusion elevated plasma glucagon in portal vein and abdominal aorta of coldacclimated rats under anesthesia (KUROSHIMA et al, 1983). In the latter experiment, however, NA infusion did not affect the glucagon levels in WC in contrast to the significant increases in the present result.…”

Section: Discussionsupporting

confidence: 91%

Effect of noradrenaline on plasma hormones and metabolites in cold-acclimated rats.

1988

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The effects of noradrenaline (NA) injection (40µg/100g, i.p.) on plasma glucagon, corticosterone (CS), deoxycorticosterone (DOCS), glucose, and free fatty acids (FFA) were investigated in cold-acclimated rats (CA) and warm controls (WC). The CA were transferred to warm control temperature ca. 18 h prior to NA or saline injection. The animals were decapitated and the trunk blood was collected 0, 10, 20, and 40 min after the injection. Plasma glucagon level increased significantly during the experimental period after NA, while saline did not influence its level. The magnitude of increase as assessed by 95% confidence interval was significantly greater in CA than in WC. Plasma CS and DOCS were significantly increased by saline injection, but NA caused greater elevations of these steroid-hormones. The magnitudes of increases were also greater in CA. In contrast to the hormonal responses, NA-induced increases of plasma glucose and FFA levels were smaller in CA than in WC. These results suggest that glucagon and glucocorticoids are released, at least partly, by NA, and these thermogenic factors act in synergism, enhancing nonshivering thermogenesis through an accelerated utilization of energy substrates such as glucose and FFA.

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Section: Discussionsupporting

confidence: 91%

Effect of noradrenaline on plasma hormones and metabolites in cold-acclimated rats.

1988

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“…In other words, the rapid increase in body temperature associated with increased thermogenesis due to exercise training is similar to a state of intermittent mild heat exposure. As heat exposure has been reported to have an inhibitory effect on norepinephrine (NE)-dependent non-shivering thermogenesis (NST) [ 42 ], it is possible that the increase in body temperature due to strength training also inhibited the increase in BAT-d in this study. As BAT is essentially an adaptive thermogenic tissue in cold environments, the attenuated increase in BAT-d as a whole in this study might be a reasonable outcome.…”

Section: Discussionmentioning

confidence: 89%

The Effects of 10-Week Strength Training in the Winter on Brown-like Adipose Tissue Vascular Density

Tanaka

Fuse-Hamaoka

Kuroiwa

et al. 2022

IJERPH

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There is no evidence of the effect of exercise training on human brown-like adipose tissue vascular density (BAT-d). Here, we report whether whole-body strength training (ST) in a cold environment increased BAT-d. The participants were 18 men aged 20–31 years. They were randomly assigned to two groups: one that performed ST twice a week at 75% intensity of one-repetition maximum for 10 weeks during winter (EX; n = 9) and a control group that did not perform ST (CT; n = 9). The total hemoglobin concentration in the supraclavicular region determined by time-resolved near-infrared spectroscopy was used as a parameter of BAT-d. ST volume (Tvol) was defined as the mean of the weight x repetition x sets of seven training movements. The number of occasions where the room temperature was lower than the median (NRcold) was counted as an index of potential cold exposure during ST. There was no significant between-group difference in BAT-d. Multiple regression analysis using body mass index, body fat percentage, NRcold, and Tvol as independent variables revealed that NRcold and Tvol were determined as predictive of changes in BAT-d. An appropriate combination of ST with cold environments could be an effective strategy for modulating BAT.

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“…In agreement with these reports, the present experiments further confirmed that the increased amylase activity was correlated well with the higher plasma insulin concentration due to heat exposure. It was reported in a previous study that the plasma insulin and glucose concentrations were low in non-starved, heat-exposed rats Kuroshima, Habara & Ohno, 1983). Accordingly, the present experiment had been first designed to expect suppression of amylase release due to the decreased insulin concentration.…”

Section: Discussionmentioning

confidence: 98%

Augmentation of secretagogue‐induced amylase secretion in pancreatic acini of heat‐exposed rats.

Habara

1989

The Journal of Physiology

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SUMMARY1. The effects of prolonged heat exposure on pancreatic exocrine secretion were investigated to evaluate the involvement of the insulin-pancreatic acinar axis. Rats were kept at 34°C and a relative humidity of 40 % for 2 weeks with or without insulin administration. Control rats were housed at the thermoneutral temperature of 25 'C. By using isolated acini, secretory function was examined at the cellular level.2. Without insulin treatment, acinar amylase concentration, expressed per microgram of cellular protein, was increased by heat exposure, while trypsinogen concentration, expressed per microgram of acinar DNA, decreased. The ratio of acinar amylase to trypsinogen increased significantly from 2-82 to 5-69 by prolonged heat exposure. With insulin treatment, the heat-induced increase in amylase activity was lessened but the decrease in trypsinogen remained unchanged. The ratio was somewhat lessened to 4-66. 3. In acini from saline-treated rats, amylase release in response to varying concentrations of cholecystokinin octapeptide or carbamylcholine was significantly augmented by prolonged heat exposure. As a result, the dose-response curve shifted upwards. However, in acini from insulin-treated rats, the increase in secretory response was lessened, similar to the effect on acinar content. On the other hand, changes in trypsinogen release were not as notable as those in amylase release. The ratio of amylase to trypsinogen in pancreatic juice released by 100 pM-cholecystokinin octapeptide increased from 1-56 to 3 04 in saline-treated rats and from 1-60 to 2-34 in insulin-treated rats.4. In heat-exposed, saline-treated rats the plasma concentrations of glucose and insulin were significantly elevated, while in insulin-treated rats these increases were lessened and the elevation of plasma insulin concentration was no longer significant. 5. It is suggested that heat exposure elevates resting plasma glucose concentration, probably because of decreased metabolic activity, which results in a concomitant rise in plasma insulin concentration. This hormonal change most likely is a major cause of augmentation of acinar amylase synthesis and of the resultant potentiation of stimulus-secretion coupling via an insulin-pancreatic acinar axis. Heat exposure modified pancreatic exocrine function in the opposite direction to what occurred in cold-exposed animals. It was confirmed that changes in pancreatic exocrine function via a modification of the insulin-pancreatic acinar axis can actually occur under normal physiological circumstances. From the nutritional point of view, this modification by ambient temperature should be taken into consideration.

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Noradrenaline-induced secretions of pancreatic hormones in cold- and heat-acclimated rats.

Cited by 5 publications

References 25 publications

Effect of noradrenaline on plasma hormones and metabolites in cold-acclimated rats.

Effect of noradrenaline on plasma hormones and metabolites in cold-acclimated rats.

The Effects of 10-Week Strength Training in the Winter on Brown-like Adipose Tissue Vascular Density

Augmentation of secretagogue‐induced amylase secretion in pancreatic acini of heat‐exposed rats.

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