Influences of Graded Dose of Melatonin on the Levels of Blood Glucose and Adrenal Catecholamines in Male Roseringed Parakeets (<i>Psittacula krameri</i>) under Different Photoperiods

Maitra, Saumen Kumar; Dey, Mamata; Dutta, Sayanta; Bhattacharya, Samir; Dey, Ruma; Sengupta, Atanu

doi:10.1076/apab.108.5.444.4297

Cited by 11 publications

(4 citation statements)

References 19 publications

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“…In our study, MT significantly decreased serum glucose level in diabetic rats which is in agreement with previous reports (26,27). This hypoglycemic effect of MT might be due to its role on catecholaminergic responses (28). Also, based on our results, treatment of STZ-induced diabetic rats with three doses of MT increased the gastric antioxidant capacity in a dosedependent manner.…”

Section: Discussionsupporting

confidence: 93%

The Effect of Melatonin Against Gastric Oxidative Stress and Dyslipidemia in Streptozotocin-Induced Diabetic Rats

et al. 2018

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Objective. The aim of this study was to evaluate the possible protective effects of MT against gastric oxidative stress and dyslipidemia in streptozotocin (STZ)-induced diabetic rats. Methods. Forty male Wistar rats were randomly divided into five groups: control, diabetic, MT 5 mg/kg+ STZ, MT 10 mg/kg+ STZ and MT 20 mg/kg+ STZ. STZ (60 mg/kg) was intraperitoneally (ip) injected as a single dose for diabetes induction. One week after STZ administration, MT was injected daily as ip for 14 days. The levels of malondialdehyde (MDA), total thiol and glutathione, as well as superoxide dismutase (SOD) and catalase activities were measured in gastric tissue. Serum concentrations of triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL) and low density lipoprotein (LDL) were also determined. Results. Serum glucose significantly increased in diabetic group compared to control group. STZ induced a significant decrease in gastric tissue levels of total thiol, glutathione, catalase and SOD activities and a significant increase in MDA concentration. In diabetic rats, serum TG, LDL and TC were significantly higher and HDL was significantly lower than in the control group. Treatment of diabetic rats with MT caused a significant increase in gastric total thiol content and glutathione concentration as well as SOD and catalase activities. Gastric MDA concentration and serum LDL, TG and TC were significantly lower in MTtreated groups when compared with diabetic group. Conclusion. These data suggested that MT has a therapeutic effect on gastric oxidative damage and dyslipidemia induced by diabetes that possibly may be due to its antioxidant effects.

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Section: Discussionsupporting

confidence: 93%

The Effect of Melatonin Against Gastric Oxidative Stress and Dyslipidemia in Streptozotocin-Induced Diabetic Rats

et al. 2018

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“…For example, melatonin caused hyperglycemia in newborn pigeons, whereas, in the adult bird, hypoglycemia was detected [65]. In budgerigars, after melatonin application under natural light conditions, as well as under long‐day conditions, hyperglycemia was observed in contrast to short‐day conditions, which caused hypoglycemia [66, 67]. In addition to the duration of the photoperiod, the divergent amounts of melatonin given or the time of day should significantly influence the effect of the pineal hormone on the glucose metabolism in birds.…”

Section: Divergent Results Characterize the History Of Melatonin–insumentioning

confidence: 99%

Melatonin, endocrine pancreas and diabetes

Peschke

2007

Journal of Pineal Research

266

254

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Melatonin influences insulin secretion both in vivo and in vitro. (i) The effects are MT(1)-and MT(2)-receptor-mediated. (ii) They are specific, high-affinity, pertussis-toxin-sensitive, G(i)-protein-coupled, leading to inhibition of the cAMP-pathway and decrease of insulin release. [Correction added after online publication 4 December 2007: in the preceding sentence, 'increase of insulin release' was changed to 'decrease of insulin release'.] Furthermore, melatonin inhibits the cGMP-pathway, possibly mediated by MT(2) receptors. In this way, melatonin likely inhibits insulin release. A third system, the IP(3)-pathway, is mediated by G(q)-proteins, phospholipase C and IP(3), which mobilize Ca(2+) from intracellular stores, with a resultant increase in insulin. (iii) Insulin secretion in vivo, as well as from isolated islets, exhibits a circadian rhythm. This rhythm, which is apparently generated within the islets, is influenced by melatonin, which induces a phase shift in insulin secretion. (iv) Observation of the circadian expression of clock genes in the pancreas could possibly be an indication of the generation of circadian rhythms in the pancreatic islets themselves. (v) Melatonin influences diabetes and associated metabolic disturbances. The diabetogens, alloxan and streptozotocin, lead to selective destruction of beta-cells through their accumulation in these cells, where they induce the generation of ROS. Beta-cells are very susceptible to oxidative stress because they possess only low-antioxidative capacity. Results suggest that melatonin in pharmacological doses provides protection against ROS. (vi) Finally, melatonin levels in plasma, as well as the arylalkylamine-N-acetyltransferase (AANAT) activity, are lower in diabetic than in nondiabetic rats and humans. In contrast, in the pineal gland, the AANAT mRNA is increased and the insulin receptor mRNA is decreased, which indicates a close interrelationship between insulin and melatonin.

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“…In addition, diabetic patients are largely devoid of a circadian melatonin rhythm . Altogether, the cited findings clearly indicate that melatonin–insulin interactions, which are modulated and regulated by catecholamines, particularly norepinephrine , play an important role in glucose metabolism.…”

Section: Introductionmentioning

confidence: 95%

Experimental and clinical aspects of melatonin and clock genes in diabetes

Peschke

Bähr

Mühlbauer

2015

Journal of Pineal Research

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The pineal hormone melatonin influences insulin secretion, as well as glucagon and somatostatin secretion, both in vivo and in vitro. These effects are mediated by two specific, high-affinity, seven transmembrane, pertussis toxin-sensitive, Gi-protein-coupled melatonin receptors, MT1 and MT2. Both isoforms are expressed in the b-cells, a-cells as well as d-cells of the pancreatic islets of Langerhans and are involved in the modulation of insulin secretion, leading to inhibition of the adenylate cyclase-dependent cyclic adenosine monophosphate as well as cyclic guanosine monophosphate formation in pancreatic b-cells by inhibiting the soluble guanylate cyclase, probably via MT2 receptors. In this way, melatonin also likely inhibits insulin secretion, whereas using the inositol triphosphate pathway after previous blocking of Gi-proteins by pertussis toxin, melatonin increases insulin secretion. Desynchrony of receptor signaling may lead to the development of type 2 diabetes. This notion has recently been supported by genomewide association studies pinpointing variances of the MT2 receptor as a risk factor for this rapidly spreading metabolic disturbance. As melatonin is secreted in a clearly diurnal fashion, it is safe to assume that it also has a diurnal impact on the blood-glucose-regulating function of the islet. Observations of the circadian expression of clock genes (Clock, Bmal1, Per1,2,3, and Cry1,2) in pancreatic islets, as well as in INS1 rat insulinoma cells, may indicate that circadian rhythms are generated in the b-cells themselves. The circadian secretion of insulin from pancreatic islets is clock-driven. Disruption of circadian rhythms and clock function leads to metabolic disturbances, for example, type 2 diabetes. The study of melatonin-insulin interactions in diabetic rat models has revealed an inverse relationship between these two hormones. Both type 2 diabetic rats and patients exhibit decreased melatonin levels and slightly increased insulin levels, whereas type 1 diabetic rats show extremely reduced levels or the absence of insulin, but statistically significant increases in melatonin levels. Briefly, an increase in melatonin levels leads to a decrease in stimulated insulin secretion and vice versa. Melatonin levels in blood plasma, as well as the activity of the key enzyme of melatonin synthesis, AA-NAT (arylalkylamine-N-acetyltransferase) in pineal, are lower in type 2 diabetic rats compared to controls. In contrast, melatonin and pineal AA-NAT mRNA are increased and insulin receptor mRNA is decreased in type 1 diabetic rats, which also indicates a close relationship between insulin and melatonin. As an explanation, it was hypothesized that catecholamines, which reduce insulin levels and stimulate melatonin synthesis, control insulinmelatonin interactions. This conviction stems from the observation that catecholamines are increased in type 1 but are diminished in type 2 diabetes. In this context, another important line of inquiry involves the fact that melatonin protects b-cells ag...

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Influences of Graded Dose of Melatonin on the Levels of Blood Glucose and Adrenal Catecholamines in Male Roseringed Parakeets (Psittacula krameri) under Different Photoperiods

Cited by 11 publications

References 19 publications

The Effect of Melatonin Against Gastric Oxidative Stress and Dyslipidemia in Streptozotocin-Induced Diabetic Rats

The Effect of Melatonin Against Gastric Oxidative Stress and Dyslipidemia in Streptozotocin-Induced Diabetic Rats

Melatonin, endocrine pancreas and diabetes

Experimental and clinical aspects of melatonin and clock genes in diabetes

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