Feeding of tobacco blend or nicotine induced weight loss associated with decreased adipocyte size and increased physical activity in male mice

Liu, Mingxia; Key, Chia-Chi Chuang; Weckerle, Allison; Boudyguina, Elena; Sawyer, Janet K.; Gebre, Abraham K.; Spoo, Wayne; Makwana, Om; Parks, John S.

doi:10.1016/j.fct.2018.01.058

Cited by 10 publications

(14 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, when nicotine treatment occurred on days 5-10, it mainly acted on mature adipocytes. Nicotine treatment reduced body weight and fat mass, and increased brown adipose tissue thermogenesis in adult rats [3,21]. According to Arai et al [22], continuous nicotine infusion stimulated UCP1 mRNA expression in the BAT of male adult Wistar rats, and it was speculated that direct nicotine exposure (as in active smoking) activates beige-like function, increases UCP1-induced thermogenesis in adipose tissue, and finally leads to body weight loss.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Nicotine induces a dual effect on the beige-like phenotype in adipocytes

Chen

Xiang

Zhang

et al. 2019

ARCH BIOL SCI BELGRA

View full text Add to dashboard Cite

Nicotine, the main component of cigarette smoke, affects white/brown adipocytes. Few studies have concentrated on beige adipocytes. In this study, 3T3-L1 cells were differentiated in the presence of nicotine (25, 50 and 100 µmol/L) during early differentiation and maintenance stages. Cell viability and the state of lipid droplets were assessed by the MTT assay and Oil Red O, respectively, and the expression of beige-related genes and proteins was examined by RT-qPCR, Western blotting and flow cytometry. Nicotine did not alter adipocyte differentiation; however, it increased the expression of peroxisome proliferator-activated receptor gamma (PPARγ) protein during early differentiation and maintenance. Nicotine treatment during early differentiation downregulated gene and protein expression of PPARγ coactivator 1-alpha (PGC-1α), uncoupling protein 1 (UCP1) and cluster of differentiation 137 (CD137), and gene expression of Cbp/p300 interacting transactivator with Glu/ Asp rich carboxy-terminal domain 1 (Cited1), transmembrane protein 26 (Tmem26), and short stature homeobox 2 (Shox2). Nicotine treatment during the maintenance stage upregulated these beige-related genes/proteins. Nicotine treatment of immature adipocytes damaged beige function through a decrease in PGC-1α/UCP1 expression, but nicotine treatment of mature adipocytes or both immature and mature cells enhanced beige functioning. Nicotine induced beige-like phenotype dysfunction in 3T3-L1 adipocytes. This process may affect thermogenesis in adipose tissue and cause a dysfunction in fat metabolism.

show abstract

Section: Discussionmentioning

confidence: 99%

“…For example, increased white fat and adipogenesis have been observed in nicotine-exposed prenatal rats [2]. In addition, direct nicotine exposure has been shown to reduce adipose weight, adipocyte size, and to induce adipose tissue triglyceride lipolysis [3]. However, the underlying mechanisms are still not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Nicotine induces a dual effect on the beige-like phenotype in adipocytes

Chen

Xiang

Zhang

et al. 2019

ARCH BIOL SCI BELGRA

View full text Add to dashboard Cite

show abstract

“…Nicotine as a sympathomimetic agent, is responsible for the decrease of appetite, raising the resting metabolic rate and lipolysis. Catecholamine production, increased by nicotine, may limit the body weight gain even without the decrease in food intake [3,15,25]. Sympathomimetic drugs increase the energy expenditure by effecting the peripheral tissue and through regulation of metabolism in the brain.…”

Section: Discussionmentioning

confidence: 99%

Lower weight gain after vaping cessation than after smoking quitting

Wawryk‐Gawda

Zarobkiewicz

Chylińska-Wrzos

et al. 2019

Rocz Panstw Zakl Hig

View full text Add to dashboard Cite

Background.Smoking is frequently a way to control appetite and weight. The data concerning the body mass gain after quitting among the users of electronic cigarettes who have no prior history of smoking traditional cigarettes is inconsistent. Objective. In our study we have compared smoking and vaping impact on weight gain and glycaemia. Material and methods. 3 groups of rats were used. The group A was exposed to vapour and group B were exposed to smoke. Rats in the group C constituted the control group without nicotine exposition. Results. During 6 weeks of experiment weight gain of rats in the A and B groups was comparable, while animals from group C had gained signifi0cantly more. During 2 weeks after cessation of exposition to nicotine animals from group B gained more weight than rats of A and C group. Blood glucose was higher in group B than in groups A and C 24 h after last exposure to nicotine and 2 weeks after nicotine exposure cessation. Conclusion. Effects of vaping on weight increase is similar to smoking, but after vaping cassation weight gain is lower and comparable with nicotine nonusers. STRESZCZENIEWprowadzenie. Palenie papierosów jest często stosowaną metodą utrzymywania niskiej masy ciała i kontroli apetytu. Badania dotyczące przyrostu masy ciała wśród osób, które nigdy nie paliły tradycyjnych papierosów i zaprzestały stosowania papierosów elektronicznych są niejednoznaczne. Cel badań. W naszym badaniu porównaliśmy wpływ papierosów tradycyjnych i elektronicznych na przyrost masy ciała i poziom cukru we krwi. Materiał i metody. Do badania użyto 3 grupy szczurów. Grupa A była eksponowana na parę z podgrzania płynu papierosa elektronicznego, grupa B została poddana działaniu dymu tytoniowego. Zwierzęta grupy C stanowiły grupę kontrolną bez narażenia na nikotynę. Wyniki. W trakcie 6 tygodni trwania eksperymentu przyrost masy ciała szczurów z grupy A i B był porównywalny, natomiast zwierzęta z grupy C przybrały istotnie więcej. Podczas 2 tygodni następujących po zaprzestaniu ekspozycji zwierzęta z grupy B przybrały więcej niż szczury z grypy A i C. Glikemia była najwyższa w grupie B zarówno bezpośrednio po zakończeniu ekspozycji, jak i po 2 tygodniowej przerwie w narażeniu na nikotynę. Wnioski. Wpływ stosowania papierosów elektronicznych na przyrost masy ciała jest porównywalny do palenia papierosów tradycyjnych w trakcie ekspozycji. Natomiast po zakończeniu narażenia na pary liquidu przyrost masy ciała jest mniejszy, podobnie jak w grupie kontrolnej.Słowa kluczowe: nikotyna, papierosy, masa ciała, palenie, papierosy elektroniczne.

show abstract

“…Since inflammation was present in 6month female WAT and not at 3 weeks, this suggests that nicotine does not have a direct effect on inflammation but that augmented oxidative stress may mediate the expression of proinflammatory cytokines. One research group demonstrated that CD-1 mice fed a nicotine-containing diet for 14 weeks postnatally decreased adipocyte cell size without affecting white adipose inflammation (Liu et al, 2018). In fact, treatment with 4-HNE in 3T3-L1 cells induced inflammation by activating p38, subsequently increasing the expression of cyclooxygenase-2 (Zarrouki et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Maternal Nicotine Exposure Leads to Augmented Expression of the Antioxidant Adipose Tissue Triglyceride Lipase Long-Term in the White Adipose of Female Rat Offspring

Barra

VanDuzer

Holloway

et al. 2018

Toxicological Sciences

View full text Add to dashboard Cite

Globally, approximately 10%-25% of women smoke during pregnancy. Since nicotine is highly addictive, women may use nicotine-containing products like nicotine replacement therapies for smoking cessation, but the long-term consequences of early life exposure to nicotine remain poorly defined. Our laboratory has previously demonstrated that maternal nicotine exposed (MNE) rat offspring exhibit hypertriglyceridemia due to increased hepatic de novo lipogenesis. Hypertriglyceridemia may also be attributed to impaired white adipose tissue (WAT) lipid storage; however, the effects of MNE on WAT are not completely understood. We hypothesize that nicotine-induced alterations in adipose function (eg, lipid storage) underlie dyslipidemia in MNE adults. Female 6-month-old rats exposed to nicotine during gestation and lactation exhibited significantly decreased visceral adipocyte cell area by 40%, attributed, in part, to a 3-fold increase in adipose triglyceride lipase (ATGL) protein expression compared with vehicle. Given ATGL has antioxidant properties and in utero nicotine exposure promotes oxidative stress in various tissues, we next investigated if there was evidence of increased oxidative stress in MNE WAT. At both 3 weeks and 6 months, MNE offspring expressed 37%-48% higher protein levels of superoxide dismutase-1 and -2 in WAT. Since oxidative stress can induce inflammation, we examined the inflammatory profile of WAT and found increased expression of cytokines (interleukin-1β, tumor necrosis factor α, and interleukin-6) by 44%-61% at 6 months. Collectively, this suggests that the expression of WAT ATGL may be induced to counter MNE-induced oxidative stress and inflammation. However, higher levels of ATGL would further promote lipolysis in WAT, culminating in impaired lipid storage and long-term dyslipidemia.

show abstract

Feeding of tobacco blend or nicotine induced weight loss associated with decreased adipocyte size and increased physical activity in male mice

Cited by 10 publications

References 39 publications

Nicotine induces a dual effect on the beige-like phenotype in adipocytes

Nicotine induces a dual effect on the beige-like phenotype in adipocytes

Lower weight gain after vaping cessation than after smoking quitting

Maternal Nicotine Exposure Leads to Augmented Expression of the Antioxidant Adipose Tissue Triglyceride Lipase Long-Term in the White Adipose of Female Rat Offspring

Contact Info

Product

Resources

About