Decreased α2-adrenergic receptor in the brain stem and pancreatic islets during pancreatic regeneration in weanling rats

Das, Vinita; Chathu, Finla; Paulose, C S

doi:10.1016/j.lfs.2006.04.016

Cited by 5 publications

(2 citation statements)

References 43 publications

(37 reference statements)

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“…A role for adrenergic receptors in the activation of intracellular signalling pathways that lead to mitogenic responses has been described [18,23,24], whilst abnormalities of sympathetic effects, including disturbances of leptin and β3-adrenergic receptor signalling may contribute to the development of obesity and type 2 diabetes in rodents [25]. We hypothesize that the exaggerated leptin surge [17] and increased sympathetic drive [19] we observe in offspring of obese rodents may also contribute to altered pancreatic development post-natally and promote NAFPD in this model [26]. Importantly, increased sympathetic drive has also implicated in proliferation of pancreatic cancer cells [27,28].…”

Section: Discussionmentioning

confidence: 56%

Maternal obesity programmes offspring development of non-alcoholic fatty pancreas disease

Oben

Patel

Mouralidarane

et al. 2010

Biochemical and Biophysical Research Communications

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Background and aimsThe prevalence of pancreatic adenocarcinoma (PAC) parallels rising rates of obesity and dysmetabolism, a possible link being non-alcoholic fatty pancreas disease (NAFPD). We have recently shown that maternal obesity programmes the development of a dysmetabolic and fatty liver (non-alcoholic fatty liver disease, NAFLD) phenotype in adult offspring. Since the pancreas and liver originate from the same embryonic bud, it is plausible that maternal obesity may similarly programme the development of NAFPD. Our objective was to determine the effect of maternal obesity on development of NAFPD in offspring and ascertain contributions of the intra/extra-uterine periods.MethodsFemale C57BL/6J mice were fed either a standard chow (3% fat, 7% sugar) or a hypercalorific diet (16% fat, 33% sugar) for six weeks prior to mating and throughout pregnancy and lactation. Female offspring were cross-fostered for suckling to dams on the same or opposite diet to yield four groups: offspring of lean suckled by lean dams (n = 6), offspring of obese suckled by obese dams (n = 6), offspring of lean suckled by obese dams (n = 5) and offspring of obese suckled by lean dams (n = 6). All offspring were weaned onto a standard chow diet at 21 days and sacrificed at 3 months post-partum for tissue collection.ResultsOffspring subjected to an adverse suckling environment showed significant increases in body weight, pancreatic triglyceride content, TGF-β, collagen gene expression and SBP at rest along with an enhanced restraint stress response, indicating a dysmetabolic and NAFPD phenotype.ConclusionsDevelopmental programming is involved in the pathogenesis of NAFPD and appears to be largely dependent on an adverse extra-uterine environment.

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Section: Discussionmentioning

confidence: 56%

Maternal obesity programmes offspring development of non-alcoholic fatty pancreas disease

Oben

Patel

Mouralidarane

et al. 2010

Biochemical and Biophysical Research Communications

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“…In the central system, a 2 -adrenergic receptors binding sites are existed in rat paraventricular nucleus and median eminence of hypothalamus (Pasquali et al 2000). Also a 2 -adrenergic receptors found in the olfactory tubercles, striatum and hippocampus (Sallinen et al 2007) appears to be an important modulator of noradrenergic neurotransmission (Das et al 2006). Moreover pan et al showed that a 2 -adrenergic receptors are also located in the superficial dorsal and ventral horns of the spinal cord (Pan et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Involvement of α2-adrenergic receptor in the regulation of the blood glucose level induced by immobilization stress

et al. 2014

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The blood glucose profiles were characterized after mice were forced into immobilization stress with various exposure durations. The blood glucose level was significantly enhanced by immobilization stress for 30 min or 1 h, respectively. On the other hand, the blood glucose level was not affected in the groups which were forced into immobilization stress for 2 or 4 h. We further examined the effect of yohimbine (an α2-adrenergic receptor antagonist) administered systemically or centrally in the immobilization stress model. Mice were pretreated intraperitoneally (i.p.; from 0.5 to 5 mg/kg), intracerebroventricularly (i.c.v.; from 1 to 10 µg/5 µl), or intrathecally (i.t.; from 1 to 10 µg/5 µl) with yohimbine for 10 min and then, forced into immobilization stress for 30 min. The blood glucose level was measured right after immobilization stress. We found that up-regulation of the blood glucose level induced by immobilization stress was abolished by i.p. pretreatment with yohimbine. And the immobilization stress-induced blood glucose level was not inhibited by i.c.v. or i.t. pretreatment with yohimbine at a lower dose (1 µg/5 µl). However, immobilization stress-induced blood glucose level was significantly inhibited by i.c.v. or i.t. pretreatment with yohimbine at higher doses (5 and 10 µg/5 µl). In addition, the i.p. (5 mg/kg), i.c.v. (10 µg/5 µl), or i.t. (10 µg/5 µl) pretreatment with yohimbine reduced hypothalamic glucose transporter 4 expression. The involvement of α2-adrenergic receptor in regulation of immobilization stress- induced blood glucose level was further confirmed by the i.p, i.c.v, or i.t pretreatment with idazoxan, another specific α2-adrenergic receptor antagonist. Finally, i.p., i.c.v., or i.t. pretreatment with yohimbine attenuated the blood glucose level in D-glucose-fed model. We suggest that α2-adrenergic receptors located at the peripheral, the brain and the spinal cord play important roles in the up-regulation of the blood glucose level in immobilization stress.

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Autonomic control of pancreatic beta cells: What is known on the regulation of insulin secretion and beta-cell proliferation in rodents and humans

Moullé

2022

Peptides

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Decreased α2-adrenergic receptor in the brain stem and pancreatic islets during pancreatic regeneration in weanling rats

Cited by 5 publications

References 43 publications

Maternal obesity programmes offspring development of non-alcoholic fatty pancreas disease

Maternal obesity programmes offspring development of non-alcoholic fatty pancreas disease

Involvement of α2-adrenergic receptor in the regulation of the blood glucose level induced by immobilization stress

Autonomic control of pancreatic beta cells: What is known on the regulation of insulin secretion and beta-cell proliferation in rodents and humans

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