Alterations of lipolysis and lipoprotein lipase in chronically nicotine-treated rats

Sztalryd, Carole; Hamilton, Jock S.; Horwitz, Barbara A; Johnson, Patricia R.; Kraemer, Fredric B.

doi:10.1152/ajpendo.1996.270.2.e215

Cited by 40 publications

(45 citation statements)

References 28 publications

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“…This is different from previous findings in rats, where acute nicotine infusion increased basal lipolysis and blunted the effects of lipolytic agonists. 11 These differences are probably related to the exposure of the rats to nicotine via acute infusion, compared to cigarette smoking in humans, as well as potential differences in rat compared to human adipose cell metabolism. 25,26 The results of the present study also differ from the report that nicotine increased lipolysis measured in vivo by microdialysis, suggesting the presence of nicotinic receptors; 12 however, in that study nicotine had no effect on lipolysis in isolated human adipose cells, similar to the findings of the present study.…”

Section: Discussionmentioning

confidence: 99%

Weight gain and adipose tissue metabolism after smoking cessation in women

et al. 2001

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BACKGROUND: Cigarette smoking increases the risk of cardiovascular disease, and is an important preventable cause of death and illness. One major deterrent to smoking cessation is a gain in body weight. Understanding the mechanisms that contribute to this weight gain may maximize the success of long-term smoking cessation. We hypothesized that smoking cessation is associated with an increase in adipose tissue lipoprotein lipase (AT-LPL) activity and=or a decrease in lipolysis, two metabolic factors that determine the balance between fat storage and fat utilization, and thus affect the propensity for weight gain. MATERIALS AND METHODS: Ten premenopausal women (37.1 AE 6.2 y, 31.7 AE 6.4 kg=m 2 body mass index (BMI), mean AE s.d.) participated in a 4 week smoking cessation program. Measurements of body weight, waist and hip circumferences, adipose cell metabolism and resting metabolic rate were obtained at baseline and after 4 weeks of smoking cessation. RESULTS: Of the 10 women who began the intervention, five successfully completed the smoking cessation intervention. After 4 weeks of smoking cessation, there were significant increases in body weight (95.1 AE 13.9 -97.7 AE 14.4 kg, P < 0.05), with no change in waist and hip circumferences or resting energy expenditure. Gluteal AT-LPL activity significantly increased in all women by 2.8-fold (1.65 AE 1.30 -4.72 AE 3.34 nmol=g=min, P < 0.05). Abdominal AT-LPL activity increased in four out of the five women, but did not reach statistical significance (1.14 AE 0.88 -3.50 AE 3.76 nmol=g=min, P ¼ 0.14). The increase in body weight correlated with the increase in gluteal AT-LPL activity (r ¼ 0.89, P < 0.05), as well as the baseline activity of gluteal AT-LPL (r ¼ 0.86, P ¼ 0.06). There were no changes in basal or stimulated lipolysis in the gluteal or abdominal fat depots. CONCLUSIONS: These results suggest that smoking cessation is associated with significant increases in body weight, as well as changes in adipose cell metabolism, in particular increases in AT-LPL activity. This increase in LPL activity may contribute to the increase in body weight associated with smoking cessation.

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Section: Discussionmentioning

confidence: 99%

Weight gain and adipose tissue metabolism after smoking cessation in women

et al. 2001

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“…Studies of feeding behavior reveal that smoking or nicotine administration decreases meal size, measured as the amount of food intake per meal, without substantial changes in meal number (Blaha et al, 1998;Miyata et al, 2001). Although studies of nicotineinduced changes in overall metabolic rate are more variable (Stamford et al, 1986;Sztalryd et al, 1996), nicotine administration has been shown to alter metabolic processing in humans, intact animals and in both hepatocytes and adipocytes, in vitro (Sztalryd et al, 1996;Ashakumary and Vijayammal, 1997;Arai et al, 2001). Nicotine decreases lipolysis by inhibiting lipoprotein lipase activity, decreasing triglyceride uptake and hence lessening net storage in adipose tissue (Sztalryd et al, 1996).…”

Section: Does Nicotine Affect Feeding Via Interactions At Peripheral mentioning

confidence: 99%

“…Although studies of nicotineinduced changes in overall metabolic rate are more variable (Stamford et al, 1986;Sztalryd et al, 1996), nicotine administration has been shown to alter metabolic processing in humans, intact animals and in both hepatocytes and adipocytes, in vitro (Sztalryd et al, 1996;Ashakumary and Vijayammal, 1997;Arai et al, 2001). Nicotine decreases lipolysis by inhibiting lipoprotein lipase activity, decreasing triglyceride uptake and hence lessening net storage in adipose tissue (Sztalryd et al, 1996). Activation of nicotinic receptors also induces the expression of uncoupling protein 1 (UCP1) in both white and brown adipose tissue (Arai et al, 2001).…”

Section: Does Nicotine Affect Feeding Via Interactions At Peripheral mentioning

confidence: 99%

Nicotinic receptor‐mediated effects on appetite and food intake

Jo¹,

Talmage

Role³

2002

J. Neurobiol.

278

197

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ABSTRACT:It is well known, although not well understood, that smoking and eating just do not go together. Smoking is associated with decreased food intake and lower body weight. Nicotine, administered either by smoking or by smokeless routes, is considered the major appetite-suppressing component of tobacco. Perhaps the most renowned example of nicotine's influence on appetite and feeding behavior is the significant weight gain associated with smoking cessation. This article presents an overview of the literature at, or near, the interface of nicotinic receptors and appetite regulation. We first consider some of the possible sites of nicotine's action along the complex network of neural and non-neural regulators of feeding. We then present the hypothesis that the lateral hypothalamus is a particularly important locus of the anorectic effects of nicotine. Finally, we discuss the potential role of endogenous cholinergic systems in motivational feeding, focusing on cholinergic pathways in the lateral hypothalamus.

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“…[20][21][22] Nikotin dapat meningkatkan pengeluaran katekolamin dan asetilkolin oleh sel adrenal. 23 Epinefrin dan norepinefrin selanjutnya mengaktivasi thermogenesis di jaringan lemak coklat.…”

Section: Pembahasanunclassified

EKSTRAK DAUN Nicotiana tabacum MENURUNKAN BERAT LEMAK VISCERAL PADA TIKUS DIABETES MELLITUS TIPE DUA

Suprapto

Jonathan²,

Ernanda³

et al. 2017

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AbstrakDiabetes mellitus merupakan masalah utama kesehatan di dunia dan prevalensinya selalu meningkat. Pada dosis yang tepat kandungan nikotin dari ekstrak etanol daun tembakau (Nicotiana tabacum) memiliki efek hipoglikemik sehingga berpeluang sebagai terapi alternatif untuk diabetes mellitus. Namun, efeknya pada jaringan adipose penderita diabetes mellitus belum banyak diketahui. Tujuan dari penelitian ini adalah untuk mengetahui pengaruh ekstrak etanol daun tembakau terhadap berat lemak visceral tikus model diabetes mellitus. Pada penelitian ini tikus galur Wistar dibagi menjadi 5 kelompok yaitu kontrol negatif (K-), kelompok tikus model diabetes mellitus (K+), dan tiga kelompok tikus diabetes melitus yang diberi ekstrak etanol daun tembakau 90 (P1), 180 (P2) dan 270 (P3) mg/kgBB/hari per oral selama 28 hari. Hasil penelitian menunjukkan bahwa terdapat penurunan bermakna berat lemak pada semua kelompok tikus DM yang diberi ekstrak daun tembakau dibandingkan dengan tikus DM tanpa terapi maupun tikus normal (p < 0,05). Kesimpulan penelitian adalah pemberian ekstrak etanol daun tembakau menurunkan berat lemak visceral pada tikus model DM. Penurunan berat lemak visceral kemungkinan disebabkan oleh kandungan nikotin dalam ekstrak yang dapat mengaktivasi lipolisis, menghambat lipogenesis, aktivasi thermogenesis, dan penurunan intake makan.Kata kunci: berat lemak visceral, diabetes mellitus, daun tembakau (Nicotiana tabacum). ETHANOL EXTRACT OF Nicotiana tabacum REDUCES THE VISCERAL WEIGHT OF TYPE TWO DIABETIC RATS AbstractDiabetes melllitusis the main health problem in the world and its prevalence is increasing dramatically. Tobacco leaf (Nicotiana tabacum) containing nicotine could be used as an alternative treatment for diabetes mellitus at the right dose. However, its effect on adipose tissue of diabetes mellitus model has not established well. This study aim is to observe the effect of ethanol extract of tobacco leaf to the visceral weight of diabetic rats. Rats were divided into five group normal rats (K-), diabetic rats (K+) and diabetic rats receiving ethanol extract of tobacco leaf at dose 90 (P1), 80 (P2), and 270 (P3) mg/kgBW/day orally for 28 days. Rats were sacrificed and visceral fat was weighed afterward. As the result, visceral fat of diabetic rats was less than the normal rats and diabetic rats treated with ethanol extract of tobacco leaf shown to reduce visceral weight significantly compared to normal rats (p < 0.05). Visceral weight decrement was due to nicotine effect that could induce lipolysis, inhibit lipogenesis, thermogenesis activation, and reduce food intake. Further research is needed to explore Nicotiana tabacum as an alternative treatment for diabetes mellitus.

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Alterations of lipolysis and lipoprotein lipase in chronically nicotine-treated rats

Cited by 40 publications

References 28 publications

Weight gain and adipose tissue metabolism after smoking cessation in women

Weight gain and adipose tissue metabolism after smoking cessation in women

Nicotinic receptor‐mediated effects on appetite and food intake

EKSTRAK DAUN Nicotiana tabacum MENURUNKAN BERAT LEMAK VISCERAL PADA TIKUS DIABETES MELLITUS TIPE DUA

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