pilocarpine/fetma

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Extreme obesity in female rats following prepuberal induction of lithium-pilocarpine seizures and a single injection of acepromazine.

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Seizures were induced in female Wistar albino rats at either 35 or 55 days of age with a single systemic injection of lithium (3 mEq/kg) and pilocarpine (30 mg/kg); the rats were then treated with the atypical neuroleptic acepromazine (25 mg/kg). These rats manifested progressive weight gain for the

Metabolic gene expression changes in the hippocampus of obese epileptic male rats in the pilocarpine model of temporal lobe epilepsy.

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Chronically epileptic male adult rats in the pilocarpine model of temporal lobe epilepsy (TLE), exhibited gross expansion of abdominal fat mass and significant weight gain several months after induction of status epilepticus (SE) when compared to control rats. We hypothesized that epileptogenesis

Proceedings: Effect of pilocarpine on insulin secretion in normal and obese hyperglycaemic mice (ob/ob) and in the rat.

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Detection of alterations in the levels of neuropeptides and salivary gland responses in the non-obese diabetic mouse model for autoimmune sialoadenitis.

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The salivary glands of non-obese diabetic (NOD) mice and BALB/c controls were evaluated for the stimulatory effects of the following neuropeptides; substance P (SP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY). Injection of either of the three neuropeptides in combination with

Regulation of plasma immunoreactive glucagon in obese hyperglycaemic (ob/ob) mice.

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This study examines the role of glucagon in the pathogenesis of the obese hyperglycaemic (ob/ob) syndrome in mice. Plasma C-terminal immunoreactive glucagon concentrations were measured in fed and fasted ob/ob mice at different ages between 5-40 weeks, and in 20-week-old mice after the

Hyperglycemia and Salivary Gland Dysfunction in the Non-obese Diabetic Mouse: Caveats for Preclinical Studies in Sjögren's Syndrome.

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The Non-obese Diabetic (NOD) mouse model for type I diabetes also develops some features of Sjögren's syndrome (SS). Since the source of the mice and the environment exert a strong influence on diabetes, this study investigated SS development in NOD mice obtained from two vendors. Female NOD mice

Alterations in the secretory response of non-obese diabetic (NOD) mice to muscarinic receptor stimulation.

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Salivary gland secretion in non-obese diabetic (NOD) and BALB/c mice was evaluated following stimulation with the muscarinic receptor agonist pilocarpine. Both saliva flow rates and total protein were similar in BALB/c and prediabetic NOD mice. With diabetes onset in NOD mice, the saliva flow rate

Specific expression of salivary maxi-K channel variant is augmented in diabetic mice.

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OBJECTIVE A genetically diabetic mouse strain (db/db) exhibits severe obesity and a syndrome resembling human non-insulin-dependent diabetes mellitus. Our histological study of submandibular glands revealed that the size and area of the granular convoluted tubules was substantially decreased in

Arginase 1 is involved in lacrimal hyposecretion in male NOD mice, a model of Sjögren's syndrome, regardless of dacryoadenitis status

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Key points: Few reports have explored the possibility of involvement of non-inflammatory factors in lacrimal hyposecretion in Sjögren's syndrome (SS). RNA-seq analysis revealed that only 4 genes, including arginase 1, were downregulated

Local expression of tumor necrosis factor-receptor 1:immunoglobulin G can induce salivary gland dysfunction in a murine model of Sjögren's syndrome.

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BACKGROUND Tumor necrosis factor is a pleiotropic cytokine with potent immune regulatory functions. Although tumor necrosis factor inhibitors have demonstrated great utility in treating other autoimmune diseases, such as rheumatoid arthritis, there are conflicting results in Sjögren's syndrome. The

E2F1-deficient NOD/SCID mice are an experimental model for dry mouth.

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Saliva contains a wide variety of secretory proteins, including alpha-amylase, lysozyme, peroxidase, immunoglobulins, and mucins. Hyposecretion of saliva and consequent dry mouth will lead to severe dental caries, periodontal disease, and mucosal infections, resulting in degrade of quality of life.

Insidious weight gain in prepubertal seized rats treated with an atypical neuroleptic: the role of food consumption, fluid consumption, and spontaneous ambulatory activity.

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Extreme obesity slowly develops in female rats over the months following seizures induced by a single systemic injection of lithium and pilocarpine if the resulting limbic seizures are treated with the atypical neuroleptic acepromazine (but not with ketamine). To discern the contributions from food

E2f1-deficient NOD/SCID mice have dry mouth due to a change of acinar/duct structure and the down-regulation of AQP5 in the salivary gland.

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Non-obese diabetic (NOD) mice have been used as a model for dry mouth. NOD mice lacking the gene encoding E2f1, a transcription factor, develop hyposalivation more rapidly progressively than control NOD mice. However, the model mice are associated with an underlying disease such as diabetes. We have

Stem cells from exfoliated deciduous teeth alleviate hyposalivation caused by Sjögren syndrome.

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To evaluate the effect of stem cells from exfoliated deciduous teeth on the hyposalivation caused by Sjögren syndrome (SS) and investigate the mechanism.Stem cells were injected into the tail veins of non-obese diabetic mice, the animal model of SS. The

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