The melanocortin receptor in the rat lacrimal gland: a model system for the study of MSH (melanocyte stimulating hormone) as a potential neurotransmitter

Leiba, Hana; Garty, Nira B.; Schmidt-Sole, Josepha; Piterman, Orly; Azrad, Anat; Salomon, Yoram

doi:10.1016/0014-2999(90)90246-3

Cited by 32 publications

(14 citation statements)

References 22 publications

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“…The MC4 receptor does not seem to be involved in the orexigenic or anorexigenic effects of neuropeptide Y (NPY), peptide YY (PYY), orexins and urocortin, as the response to these neuropeptides on food intake is normal in MC4 receptor À/À (Marsh et al, 1999a;Halatchev et al, 2004). On the other hand, cholecystokinin (CCK), a gut-derived satiety factor has an attenuated response (inhibiting food intake) in MC4 À/À (Fan et al, (Thody et al, 1976;Leiba et al, 1990;Robbins et al, 1993;Bhardwaj et al, 1997;Lipton and Catania, 1998;Boston, 1999;Gantz and Fong, 2003) Abbreviations: ACTH, adrenocoticotropic hormone; AgRP, agouti-related protein; MC, melanocortin; MCR, melanocortin receptor; MSH, melanocyte-stimulating hormone.…”

Section: Introductionmentioning

confidence: 99%

The MC4 receptor and control of appetite

Adan

Tiesjema

Hillebrand

et al. 2006

British J Pharmacology

229

157

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Mutations in the human melanocortin (MC)4 receptor have been associated with obesity, which underscores the relevance of this receptor as a drug target to treat obesity. Infusion of MC4R agonists decreases food intake, whereas inhibition of MC receptor activity by infusion of an MC receptor antagonist or with the inverse agonist AgRP results in increased food intake. This review addresses the role of the MC system in different aspects of feeding behaviour. MC4R activity affects meal size and meal choice, but not meal frequency, and the type of diet affects the efficacy of MC4R agonists to reduce food intake. The central sites involved in the different aspects of feeding behaviour that are affected by MC4R signalling are being unravelled. The paraventricular nucleus plays an important role in food intake per se, whereas MC signalling in the lateral hypothalamus is associated with the response to a high fat diet. MC4R signalling in the brainstem has been shown to affect meal size. Further genetic, behavioural and brain-region specific studies need to clarify how the MC4R agonists affect feeding behaviour in order to determine which obese individuals would benefit most from treatment with these drugs. Application of MCR agonists in humans has already revealed side effects, such as penile erections, which may complicate introduction of these drugs in the treatment of obesity.

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Section: Introductionmentioning

confidence: 99%

The MC4 receptor and control of appetite

Adan

Tiesjema

Hillebrand

et al. 2006

British J Pharmacology

229

157

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“…α-MSH binds to the MCRs to mediate physiological functions, including metabolic regulation 15 and neuroprotection 16 17 in the brain. In the eye, the MCRs are widely distributed in the ocular surface tissues, including, but not limited to, the acinar cells in extraorbital and intraorbital lachrimal glands 18 . α-MSH binds to these receptors with specificity and affinity 18 19 , and promotes the protein secretion from the in vitro lacrimal gland preparation 18 .…”

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confidence: 99%

α-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways

Huang

Liu

et al. 2015

Sci Rep

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Dry eye is a highly prevalent, chronic, and multifactorial disease that compromises quality of life and generates socioeconomic burdens. The pathogenic factors of dry eye disease (DED) include tear secretion abnormalities, tear film instability, and ocular surface inflammation. An effective intervention targeting the pathogenic factors is needed to control this disease. Here we applied α-Melanocyte-stimulating hormone (α-MSH) twice a day to the ocular surface of a scopolamine-induced dry eye rat model. The results showed that α-MSH at different doses ameliorated tear secretion, tear film stability, and corneal integrity, and corrected overexpression of proinflammatory factors, TNF-α, IL-1β, and IFN-γ, in ocular surface of the dry eye rats. Moreover, α-MSH, at 10−4 μg/μl, maintained corneal morphology, inhibited apoptosis, and restored the number and size of conjunctival goblet cells in the dry eye rats. Mechanistically, α-MSH activated both PKA-CREB and MEK-Erk pathways in the dry eye corneas and conjunctivas; pharmacological blockade of either pathway abolished α-MSH’s protective effects, suggesting that both pathways are necessary for α-MSH’s protection under dry eye condition. The peliotropic protective functions and explicit signaling mechanism of α-MSH warrant translation of the α-MSH-containing eye drop into a novel and effective intervention to DED.

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“…It is also reported to more influences, as treatment of various skin disorders including inflammatory dermatoses [19] , modulates local and circulating tumor necrosis factor (TNF) in experimental brain inflammation [20] , this hormone can inhibit the induction of contact hypersensitivity reactions and to induce hapten-specific tolerance [21] , anti-inflammatory and anti-invasive effects in human melanoma cells [22] , the antiinflammatory actions of the peptide via peripheral and /or central melanocortin receptors might put the peptide into practice therapeutically in near future [23] . More studies suggest that -MSH, decrease body fat in humans [24] as a potential neurotransmitter [25] , regulate energy balance, appetite control, as well as glucose transport in rat adipocytes [26] .…”

Section: Introductionmentioning

confidence: 99%

Effects of Administration of Alpha-Melanocyte Stimulating Hormone (α-MSH) on Some Hematological Values of Alloxan-induced Diabetic Rats

Mansi¹

2006

American J. of Pharmacology and Toxicology

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This study was designed to evaluate the role of alpha-melanocyte stimulating hormone ( -MSH) on heart rate and some hematological values in alloxan induced diabetic rats. 40 male white rats were divided into four experimental groups: control, diabetic, -MSH-treated and -MSH-treated diabetic. At the end of the experimental period (3weeks), animals in all four groups were fasted for 12 hrs and blood samples were taken for the determination of plasma insulin, Glucagon, glucose levels, RBC and WBC (red and white blood cell) counts, packed cell volume (PCV), erythrocyte sedimentation rate (ESR) and hemoglobin (Hb) concentration. It was found that ( -MSH) increased the lowered RBC and WBC counts, PCV and neutrophil percentage in diabetic rats. However the WBC counts of the ( -MSH) treated diabetic group was still lower than the control and ( -MSH) group. ( -MSH) also decreased the elevated heart rate, ESR and glucose concentration of diabetic rats. The hormone was investigated for hypoglycemic effect in diabetic rats and induced not significant reduction in serum glucose from (19.83±1.25 MmolL) in diabetic group to (15.7±1.10 MmolL) in ( -MSH)-treated diabetic group. However the blood glucose still higher than the control and ( -MSH) group, serum insulin increased from (0.55±0.08 ng mL 1 ) in control group to (0.65±0.06 ng mL 1 ) in -MSH-treated group and still higher than control in -MSH-treated diabetic (0.59±042 ng mL 1 ) and serum Glucagon increased in diabetic, -MSH-treated and -MSH-treated diabetic groups. It is concluded that treatment ( -MSH) might decrease the diabetes-induced disturbances of heart rate and some hematological parameters of alloxan-induced diabetic rats.

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The melanocortin receptor in the rat lacrimal gland: a model system for the study of MSH (melanocyte stimulating hormone) as a potential neurotransmitter

Cited by 32 publications

References 22 publications

The MC4 receptor and control of appetite

The MC4 receptor and control of appetite

α-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways

Effects of Administration of Alpha-Melanocyte Stimulating Hormone (α-MSH) on Some Hematological Values of Alloxan-induced Diabetic Rats

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