Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1564-E1571 ◽  
Author(s):  
Hui Chen ◽  
Michelle J. Hansen ◽  
Jessica E. Jones ◽  
Ross Vlahos ◽  
Gary P. Anderson ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Caloric Intake ◽  
Fold Increase ◽  
Smoke Exposure ◽  
Metabolic Effects ◽  
Cigarette Smoke Exposure ◽  
High Fat ◽  
Fat Accumulation ◽  
Reduced Body ◽  
Plasma Leptin

Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation.

scholarly journals The Lung Inflammation and Skeletal Muscle Wasting Induced by Subchronic Cigarette Smoke Exposure Are Not Altered by a High-Fat Diet in Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80471 ◽  
Author(s):  
Michelle J. Hansen ◽  
Hui Chen ◽  
Jessica E. Jones ◽  
Shenna Y. Langenbach ◽  
Ross Vlahos ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cigarette Smoke ◽  
High Fat Diet ◽  
Lung Inflammation ◽  
Muscle Wasting ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
High Fat ◽  
Skeletal Muscle Wasting

Transgenic MSH overexpression attenuates the metabolic effects of a high-fat diet

2007 ◽  
Vol 293 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
Michelle Lee ◽  
Andrea Kim ◽  
Streamson C. Chua ◽  
Silvana Obici ◽  
Sharon L. Wardlaw
Keyword(s):  
High Fat Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Fat Percentage ◽  
Male And Female ◽  
Fat Accumulation ◽  
Low Fat Diet ◽  
Hepatic Fat ◽  
Biochemical Analyses

To determine whether long-term melanocortinergic activation can attenuate the metabolic effects of a high fat diet, mice overexpressing an NH2-terminal POMC transgene that includes α- and γ3-MSH were studied on either a 10% low-fat diet (LFD) or 45% high-fat diet (HFD). Weight gain was modestly reduced in transgenic (Tg-MSH) male and female mice vs. wild type (WT) on HFD ( P < 0.05) but not LFD. Substantial reductions in body fat percentage were found in both male and female Tg-MSH mice on LFD ( P < 0.05) and were more pronounced on HFD ( P < 0.001). These changes occurred in the absence of significant feeding differences in most groups, consistent with effects of Tg-MSH on energy expenditure and partitioning. This is supported by indirect calorimetry studies demonstrating higher resting oxygen consumption and lower RQ in Tg-MSH mice on the HFD. Tg-MSH mice had lower fasting insulin levels and improved glucose tolerance on both diets. Histological and biochemical analyses revealed that hepatic fat accumulation was markedly reduced in Tg-MSH mice on the HFD. Tg-MSH also attenuated the increase in corticosterone induced by the HFD. Higher levels of Agrp mRNA, which might counteract effects of the transgene, were measured in Tg-MSH mice on LFD ( P = 0.02) but not HFD. These data show that long-term melanocortin activation reduces body weight, adiposity, and hepatic fat accumulation and improves glucose metabolism, particularly in the setting of diet-induced obesity. Our results suggest that long-term melanocortinergic activation could serve as a potential strategy for the treatment of obesity and its deleterious metabolic consequences.

scholarly journals Hepatic Transcriptome Profiling Reveals Lack of Acsm3 Expression in Polydactylous Rats with High-Fat Diet-Induced Hypertriglyceridemia and Visceral Fat Accumulation

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1462
Author(s):  
Kristýna Junková ◽  
Lukáš F. Mirchi ◽  
Blanka Chylíková ◽  
Michaela Janků ◽  
Jan Šilhavý ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Spontaneously Hypertensive Rat ◽  
Tricarboxylic Acid Cycle ◽  
Caloric Intake ◽  
Transcriptome Profiling ◽  
Brown Norway ◽  
High Fat ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

Metabolic syndrome (MetS) is an important cause of worldwide morbidity and mortality. Its complex pathogenesis includes, on the one hand, sedentary lifestyle and high caloric intake, and, on the other hand, there is a clear genetic predisposition. PD (Polydactylous rat) is an animal model of hypertriglyceridemia, insulin resistance, and obesity. To unravel the genetic and pathophysiologic background of this phenotype, we compared morphometric and metabolic parameters as well as liver transcriptomes among PD, spontaneously hypertensive rat, and Brown Norway (BN) strains fed a high-fat diet (HFD). After 4 weeks of HFD, PD rats displayed marked hypertriglyceridemia but without the expected hepatic steatosis. Moreover, the PD strain showed significant weight gain, including increased weight of retroperitoneal and epididymal fat pads, and impaired glucose tolerance. In the liver transcriptome, we found 5480 differentially expressed genes, which were enriched for pathways involved in fatty acid beta and omega oxidation, glucocorticoid metabolism, oxidative stress, complement activation, triacylglycerol and lipid droplets synthesis, focal adhesion, prostaglandin synthesis, interferon signaling, and tricarboxylic acid cycle pathways. Interestingly, the PD strain, contrary to SHR and BN rats, did not express the Acsm3 (acyl-CoA synthetase medium-chain family member 3) gene in the liver. Together, these results suggest disturbances in fatty acid utilization as a molecular mechanism predisposing PD rats to hypertriglyceridemia and fat accumulation.

Abstract 293: Id3 Regulates High-Fat-Diet--Induced IgG2c Production

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Daniel B Harmon ◽  
Stephanie N Oldham ◽  
Loren D Erickson ◽  
Coleen A McNamara
Keyword(s):  
Adipose Tissue ◽  
B Cells ◽  
B Cell ◽  
High Fat Diet ◽  
Fold Increase ◽  
Cell Number ◽  
Metabolic Effects ◽  
High Fat ◽  
Helix Loop Helix

Background: High-fat diet (HFD)-induced adipose tissue inflammation leads to insulin resistance and glucose intolerance, increasing the risk of cardiovascular disease. Recently, B cells and IgG antibodies have been shown to promote the metabolic consequences of obesity. HFD induces IgG2c production - an IgG isotype that promotes inflammatory disorders. Mice null for Id3, a helix-loop-helix protein known to mediate IgG2c responses in vivo, develop significantly attenuated HFD-induced obesity; raising the interesting hypothesis that Id3 promotes HFD-induced obesity by mediating HFD-induced IgG2c production. Methods and results: Western Blot analysis revealed that primary splenic B cells stimulated with IFN + CD40L (an IgG2c-inducing cocktail) expressed significantly greater amounts of Id3 protein compared to B cells treated with CD40L alone ((1.26+/-0.05 vs 0.88+/-0.03; n=3; p=0.003). ELISA determination of immunoglobulin levels from whole adipose tissue of fed C57Bl/6J (WT) mice fed a HFD (60% kcal fat) revealed a 4 fold increase in IgG2c (3810+/-789 ng vs 993+/-422 ng; n=5; p=0.01) - but not IgM, IgG1, or IgG2b - compared to chow-fed controls. No differences in serum IgG2c were observed. In contrast, HFD-induced adipose tissue IgG2c levels were significantly attenuated in Id3 -/- mice (1643+/-493 vs 889+/-272 ng; n=6-7; p=0.19), despite the fact that Id3 -/- mice had significantly more adipose tissue B cells per (g) fat compared to WT (1.6E5+/-0.2E5 vs 0.5E5+/-0.09E5; n=5; p=0.001). Conclusions: Id3 promotes HFD-induced local adipose tissue IgG2c production; an effect not dependent on B cell number. Studies in animals with B cell-specific loss of Id3 are ongoing to identify the mechanisms whereby Id3 mediates HFD-induced IgG2c production and downstream metabolic effects.

Uridine attenuates obesity, ameliorates hepatic lipid accumulation and modifies the gut microbiota composition in mice fed with a high-fat diet

2021 ◽  
Author(s):  
Yilin Liu ◽  
Chunyan Xie ◽  
Zhenya Zhai ◽  
Ze-yuan Deng ◽  
Hugo R. De Jonge ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Microbiota Composition ◽  
High Fat ◽  
Fat Accumulation ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Gut Microbiota Composition

This study aimed to investigate the effect of uridine on obesity, fat accumulation in liver, and gut microbiota composition in high-fat diet-fed mice.

High-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and cholecystokinin: implications for circulatory control

2011 ◽  
Vol 300 (3) ◽  
pp. H961-H967 ◽  
Author(s):  
Jackie M. Y. How ◽  
Barbara C. Fam ◽  
Anthony J. M. Verberne ◽  
Daniela M. Sartor
Keyword(s):  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
High Fat ◽  
Lower Plasma ◽  
Lower Tertile ◽  
Circulatory Control ◽  
Plasma Leptin

Gastric leptin and cholecystokinin (CCK) act on vagal afferents to induce cardiovascular effects and reflex inhibition of splanchnic sympathetic nerve discharge (SSND) and may act cooperatively in these responses. We sought to determine whether these effects are altered in animals that developed obesity in response to a medium high-fat diet (MHFD). Male Sprague-Dawley rats were placed on a low-fat diet (LFD; n = 8) or a MHFD ( n = 24) for 13 wk, after which the animals were anesthetized and artificially ventilated. Arterial pressure was monitored and blood was collected for the determination of plasma leptin and CCK. SSND responses to leptin (15 μg/kg) and CCK (2 μg/kg) administered close to the coeliac artery were evaluated. Collectively, MHFD animals had significantly higher plasma leptin but lower plasma CCK levels than LFD rats ( P < 0.05), and this corresponded to attenuated or reversed SSND responses to CCK (LFD, −21 ± 2%; and MHFD, −12 ± 2%; P < 0.05) and leptin (LFD, −6 ± 2%; and MHFD, 4 ± 1%; P < 0.001). Alternatively, animals on the MHFD were stratified into obesity-prone (OP; n = 8) or obesity-resistant (OR; n = 8) groups according to their weight gain falling within the upper or lower tertile, respectively. OP rats had significantly higher resting arterial pressure, adiposity, and plasma leptin but lower plasma CCK compared with LFD rats ( P < 0.05). The SSND responses to CCK or leptin were not significantly different between OP and OR animals. These results demonstrate that a high-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and CCK and may impact on sympathetic vasomotor mechanisms involved in circulatory control.

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