Nicotine treatment decreases food intake and body weight viaa leptin‐independent pathway in Psammomys obesus

Sanigorski, Andrew; Fahey, R. P.; Cameron‐Smith, David; Collier, Gregory

doi:10.1046/j.1463-1326.2002.00216.x

Cited by 17 publications

(7 citation statements)

References 21 publications

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“…Although inconsistent, there are some reports that smokers have increased blood leptin levels (Eliasson and Smith, 1999;Nicklas et al, 1999) and that chronic nicotine results in higher leptin serum concentrations in adult and prenatal animal models (Arai et al, 2001;Grove et al, 2001), which could be a mechanism for nicotine's anorexic effects. However, others have found no correlation between nicotine consumption, blood leptin levels, and decreased body weight in adult models or in mothers who smoked, questioning the significance of leptin in explaining nicotine's anorexic actions (Helland et al, 2001;Sanigorski et al, 2002).…”

Section: Leptin Does Not Regulate Body Weight In Neonatesmentioning

confidence: 99%

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Huang

Winzer‐Serhan

2007

Developmental Neurobiology

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Maternal smoking results in low birth weight. Using a neonatal gastric intubation model corresponding to the third trimester in humans, nicotine, the major psychoactive ingredient in tobacco, causes growth retardation in rat pups. Here, we wanted to determine the underlying mechanisms of nicotine's anorexic effects. In adults, body weight and energy expenditure are regulated by the adiposity hormone leptin and the orexigenic peptides neuropeptide Y (NPY) and agouti-related peptide (AgRP) and anorexic peptides proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) expressed in the hypothalamic arcuate (Arc) nucleus. Activation of nicotinic acetylcholine receptors (nAChRs) could regulate leptin release and/or peptide expression in the Arc. Neonatal rat pups were treated twice daily with nicotine (0.25, 1.5, and 3 mg/kg) from postnatal day 1 to 8 (P1-8). This resulted in an upregulation of heteromeric nAChR binding sites in the ventromedial nucleus of the hypothalamus and Arc. Nicotine at all three doses significantly reduced body weight gain and increased mRNA expression of NPY, AgRP, and POMC effects, which were blocked by dihydro-beta-erythroidine (DHbetaE), an alpha4beta2* nAChR antagonist, but CART expression was unaffected. In contrast, serum leptin levels were significantly increased only by 3 and 1.5 mg/kg, and the increase was only partially blocked by DHbetaE. These data suggest that in neonates chronic nicotine regulates body weight gain independent from serum leptin levels by a central mechanism involving alpha4beta2* heteromeric nAChRs and stimulated increased expression of the anorexic peptide POMC. Whereas, increased NPY and AgRP expression could be a secondary response to reduction in weight gain.

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Section: Leptin Does Not Regulate Body Weight In Neonatesmentioning

confidence: 99%

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Huang

Winzer‐Serhan

2007

Developmental Neurobiology

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“…Another mechanism that might be involved in our study is based on the anti-oxidative activity of CBD [13,23], that very likely prevents beta cell destruction in the HE fed Psammomys. Vanadyl sulfate and rosiglitazone have also been found to be effective in preventing hyperglycemia and hyperinsulinemia [24,25], while nicotine treatment [26] caused decrease in food intake and body weight. An antidiabetic effect was also obtained by G protein kinase analogs [27] and electroacupuncture [28].…”

Section: Open Accessmentioning

confidence: 99%

Islet protection and amelioration of diabetes type 2 in Psammomys obesus by treatment with cannabidiol

Ziv¹,

Weiss²,

Patlas

et al. 2012

JDM

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Background and purpose: Cannabidiol (CBD), a non-psychoactive component of Cannabis sativa, has been shown by us, to have an anti-inflammatory effect in collagen-induced arthritis in DBA mice and in type 1 diabetes in NOD mice. As inflammation is a process involved in diabetes type 2, we administered CBD to Psammomys obesus (sand rats), a species which develops diabetes type 2 when fed high-energy (HE) diet, to investigate whether we can hinder the development of the disease. Experimental Approach: Male Psammomys obesus were kept on a high energy diet during the experiments. They were treated with CBD (i.p injection, 5 mg/kg, 5 times/week) for 4 weeks and kept (without CBD) for another 29 - 39 days. The weights of the animals as well as blood glucose and plasma insulin levels were determined and the morphology of the pancreatic islets was examined. Key results: CBD significantly reduced blood glucose levels in Psammomys obesus, without effecting body weight. Plasma insulin levels were significantly higher in the CBD-treated group. The most striking effect noted was the marked decrease of the destruction of pancreatic islets and beta cells. Conclusions and implications: CBD partially protects pancreatic islets and beta cells from destruction. CBD lowers significantly the blood glucose level and increases insulin level in Psammomys obesus with diabetes type 2, but does not lead to obesity. As CBD already has been administered to patients for other medical indications we propose its use as a therapeutic agent in diabetes type 2

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“…It is well established from animal studies that nicotine can act within the central nervous system to decrease food intake and body weight [63-66]. Although most studies examining nicotine's effect on energy balance are acute studies performed in adult animals, there is an increasing evidence that exposure to nicotine during development can produce long lasting perturbations in brain neurochemistry including dopamine, serotonin, acetylcholine, and a variety of neuropeptides, as well as leptin receptors [67-77].…”

Section: Smoking and The Fetal Origins Of Diseasementioning

confidence: 99%

Exposure to Smoke During Development: Fetal Programming of Adult Disease

Bergen¹

2006

Tob. Induced Dis.

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It is well established that smoking has potent effects on a number of parameters including food intake, body weight, metabolism, and blood pressure. For example, it is well documented that 1) there is an inverse relationship between smoking and body weight, and 2) smoking cessation is associated with weight gain. However, there is increasing evidence that smoking can exert deleterious effects on energy balance through maternal exposure during fetal development. Specifically, there appears to be an increased incidence of metabolic disease (including obesity), and cardiovascular disease in children and adults that were exposed to smoke during fetal development. The present review will examine the relationship between maternal smoke and adult disease in offspring. The epidemiological studies highlighting this relationship will be reviewed as well as the experimental animal models that point to potential mechanisms underlying this relationship. A better understanding of how smoking effects changes in energy balance may lead to treatments to ameliorate the long-lasting effects of perinatal exposure to smoke as well as increasing the health benefits associated with smoking cessation.

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Nicotine treatment decreases food intake and body weight viaa leptin‐independent pathway in Psammomys obesus

Cited by 17 publications

References 21 publications

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Islet protection and amelioration of diabetes type 2 in <i>Psammomys obesus</i> by treatment with cannabidiol

Exposure to Smoke During Development: Fetal Programming of Adult Disease

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Nicotine treatment decreases food intake and body weight viaa leptin‐independent pathway in Psammomys obesus

Cited by 17 publications

References 21 publications

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Nicotine regulates mRNA expression of feeding peptides in the arcuate nucleus in neonatal rat pups

Islet protection and amelioration of diabetes type 2 in &lt;i&gt;Psammomys obesus&lt;/i&gt; by treatment with cannabidiol

Exposure to Smoke During Development: Fetal Programming of Adult Disease

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Islet protection and amelioration of diabetes type 2 in <i>Psammomys obesus</i> by treatment with cannabidiol