Effects of leptin, ghrelin and neuropeptide y on spike-wave discharge activity and certain biochemical parameters in WAG/Rij rats with genetic absence epilepsy

Öztaş, Berrin; Şahin, Deniz; Kır, Hale Maral; Kuşkay, Sevinç; Ateş, Nurbay

doi:10.1016/j.jneuroim.2020.577454

Cited by 4 publications

(7 citation statements)

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“…Leptin hormones interact with a receptor in the hypothalamus, suppressing hunger and stimulating satiety; this is done by interacting with several receptors such as neuropeptide Y (a hunger promoter) [ 6 ], as well as anandamide, which is another hunger promoter shared with tetrahydrocannabinol, which binds to the same receptors [ 7 ]. Moreover, it increases the synthesis of α-Melanocyte-stimulating hormone (α-MSH), which suppresses hunger; such appetite suppression is long-term.…”

Section: Resultsmentioning

confidence: 99%

Leptin hormone and its effectiveness in reproduction, metabolism, immunity, diabetes, hopes and ambitions

Al-Hussaniy¹,

Albu-Rghaif²,

Naji³

2021

JMedLife

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Leptin is a hormone derived from adipose tissue and the small intestine, mainly in enterocytes; it helps regulate the energy balance by suppressing hunger, resulting in decreased fat mass in adipocytes. Leptin has specific receptors in the ventromedial and arcuate nuclei and other parts of the hypothalamus and the feeding center in the ventral tegmental area. It also plays a role in regulatory aspects other than fat cells, such as obesity, which is linked to a loss of sensitivity of leptin receptors, resulting in an inability to produce satiety and an increase in food intake. Moreover, leptin plays a part in lactation, bone density, the immune system, diabetes treatments, and hypertriglyceridemia. The latest studies in leptin suggest that an analog of leptin may treat DM and hypertriglyceridemia. Further research should be conducted on the effectiveness of leptin on other related diseases.

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Section: Resultsmentioning

confidence: 99%

Leptin hormone and its effectiveness in reproduction, metabolism, immunity, diabetes, hopes and ambitions

Al-Hussaniy¹,

Albu-Rghaif²,

Naji³

2021

JMedLife

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“…These data imply that ghrelin might not follow a linear dose–response curve [ 113 ]. There is one study that recently demonstrated ghrelin administration to be proconvulsive in a WAG/Rij rat model presenting with absence seizures, as ghrelin increased the number of spike–wave discharges and the total seizure duration one hour after administration [ 114 ].…”

Section: Preclinical Evidence For Ghrelin As a Potential Antiseizure Drugmentioning

confidence: 99%

“…Another study showed that ghrelin administration decreased cortical TNF- α and NF-κB expression in the pilocarpine rat model [ 140 ]. However, ghrelin did not alter serum levels of galanin, fibroblast growth factor (FGF-2), IL-6, TNF-α, and IL-1β in the Wag/Rij rat model with nonconvulsive absence seizures [ 114 ].…”

Section: Molecular Mechanisms-of-actionmentioning

confidence: 99%

“…It remains unclear whether the effects of ghrelin on decreasing oxidative stress are caused directly, or because ghrelin is anticonvulsant, and the lower number of seizures leads to decreased oxidative stress. However, in the WAG/Rij rat model with nonconvulsive absence seizures, ghrelin was not anticonvulsant, but it still reduced the malondialdehyde [ 114 ].…”

Section: Molecular Mechanisms-of-actionmentioning

confidence: 99%

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Targeting the Ghrelin Receptor as a Novel Therapeutic Option for Epilepsy

et al. 2021

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Epilepsy is a neurological disease affecting more than 50 million individuals worldwide. Notwithstanding the availability of a broad array of antiseizure drugs (ASDs), 30% of patients suffer from pharmacoresistant epilepsy. This highlights the urgent need for novel therapeutic options, preferably with an emphasis on new targets, since “me too” drugs have been shown to be of no avail. One of the appealing novel targets for ASDs is the ghrelin receptor (ghrelin-R). In epilepsy patients, alterations in the plasma levels of its endogenous ligand, ghrelin, have been described, and various ghrelin-R ligands are anticonvulsant in preclinical seizure and epilepsy models. Up until now, the exact mechanism-of-action of ghrelin-R-mediated anticonvulsant effects has remained poorly understood and is further complicated by multiple downstream signaling pathways and the heteromerization properties of the receptor. This review compiles current knowledge, and discusses the potential mechanisms-of-action of the anticonvulsant effects mediated by the ghrelin-R.

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“…The KD therapy can significantly increase the production of certain neurohormones, such as leptin and cortisol (36,37). First, leptin receptors are found throughout the brain, and their stimulation leads to antiseizure effects by decreasing proinflammatory cytokines (e.g., IL-1β), increasing an endogenous anticonvulsant (galanin), and acting as an antioxidant by increasing glutathione and decreasing malondialdehyde (37)(38)(39). Second, ghrelin, neuropeptide Y, galanin, and cortisol can induce alterations in GABA uptake and serotonin turnover and affect ion channels, thereby decreasing neuronal excitability, although the exact mechanisms need to be explored by future research (20,40).…”

Section: Production Of Neurohormonesmentioning

confidence: 99%