Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet

Morris, Margaret J.; Chen, Hui; Watts, R. W. E.; Shulkes, Arthur; Cameron‐Smith, David

doi:10.1038/sj.ijo.0803716

Cited by 45 publications

(32 citation statements)

References 67 publications

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“…The PVN is a major integration site for inputs related to food intake and energy homeostasis (56). In the current study, reduced PVN and AH NPY concentration in the animals on HFD alone was consistent with previous studies in mice and rats (26,27,39). Compared with our previous 4-wk study (11), the se ϩ chow animals had lower caloric intake (23% reduction at 7 wk vs. 19% reduction at 4 wk), greater weight loss (15% at 7 wk vs. 9% at 4 wk), and larger plasma leptin reduction (38% at 7 wk vs. 18% at 4 wk).…”

Section: Discussionsupporting

confidence: 80%

“…The sham-exposed animals were handled identically but were not exposed to cigarette smoke. Mice consumed either laboratory chow (3.54 kcal/g, 12% fat, 22% protein, 66% carbohydrate; chow-fed cohort) or a HFD [4.32 kcal/g, 32% fat (17% saturated fat), 18% protein, 50% carbohydrate; HFDfed cohort] consisting of modified laboratory chow containing sweetened condensed milk and lard, which was supplemented with highly palatable cafeteria style food such as meat pies, cakes, and biscuits (26,27,39). Fresh food was provided at 1700 daily.…”

Section: Animalsmentioning

confidence: 99%

“…Changes in the expression of genes relevant to energy expenditure [uncoupling proteins (UCP)], insulin sensitivity (TNF-␣, IL-6), and ATGL in fat pads may participate in this process (11). When facing a palatable highfat diet (HFD), mice spontaneously display hyperphagia, resulting in marked fat accumulation, and reduced hypothalamic NPY (39). In this study, we investigated whether cigarette smoke exposure would alter the weight gain and metabolic risk induced by a HFD.…”

mentioning

confidence: 99%

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

Chen¹,

Hansen²,

Jones³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Morris MJ. Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice. Am J Physiol Endocrinol Metab 293: E1564-E1571, 2007. First published October 16, 2007 doi:10.1152/ajpendo.00442.2007.-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. adipose triglyceride lipase; appetite; leptin; neuropeptide Y; tumor necrosis factor-␣ WORLDWIDE, 1

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Section: Discussionsupporting

confidence: 80%

Section: Animalsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

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

Chen¹,

Hansen²,

Jones³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…In adult animals, hypothalamic NPY and POMC are downregulated in the face of HFD feeding, whereas MC4R mRNA expression is upregulated. [39][40][41] In the current study, mRNA expression of MC4R was reduced by maternal obesity. MC4R is critical for normal control of food intake, 42 as MC4R-selective agonists cause dose dependent hypophagia and weight loss, whereas MC4R-selective antagonists or MC4-R knockout cause markedly increased food intake obesity.…”

Section: Maternal Obesity and Leptin At Birth Mj Morris And H Chenmentioning

confidence: 88%

Established maternal obesity in the rat reprograms hypothalamic appetite regulators and leptin signaling at birth

2008

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Objective: Key appetite regulators and their receptors are already present in the fetal hypothalamus, and may respond to hormones such as leptin. Intrauterine food restriction or hyperglycemia can reprogram these circuits, possibly predisposing individuals to adverse health outcomes in adulthood. Given the global obesity epidemic, maternal overweight and obesity is becoming more prevalent. Earlier, we observed rapid growth of pups from obese dams during the suckling period. However, it is unclear whether this is because of alterations in leptin and hypothalamic appetite regulators at birth. Design: Female Sprague-Dawley rats were fed palatable high-fat diet (HFD) or chow for 5 weeks to induce obesity before mating. The same diet continued during gestation. At day 1, after birth, plasma and hypothalamus were collected from male and female pups. Measurements: Body weight and organ mass were recorded. Leptin and insulin levels were measured in the plasma by radioimmunoassay. Hypothalamic mRNA expression of neuropeptide-Y (NPY), pro-opiomelanocortin, leptin receptor and its downstream signal, STAT3 (signal transducer and activator of transcription 3), were measured using real-time PCR. Results: Body and organ weights of pups from obese dams were similar to those from lean dams, across both genders. However, plasma leptin levels were significantly lower in offspring from obese dams (male: 0.53±0.13 vs 1.05±0.21 ng ml À1 ; female: 0.33 ± 0.09 vs 2.12 ± 0.57 ng ml À1 , respectively; both Po0.05). Hypothalamic mRNA expression of NPY, pro-opiomelanocortin, leptin receptor and STAT3 were also significantly lower in pups from obese dams. Conclusion: Long-term maternal obesity, together with lower leptin levels in pups from obese dams may contribute to the lower expression of key appetite regulators on day 1 of life, suggesting altered intrauterine neuron development in response to intrauterine overnutrition, which may contribute to eating disorders later in life.

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“…The CD consisted of modified laboratory chow containing sweetened condensed milk and lard, which was supplemented with highly palatable cafeteria-style foods such as meat pies, pasta and cakes as described previously. [31][32][33] The UL rats were divided in the same manner, with half of the pups receiving standard chow (UC; n ¼ 13) and the other half receiving CD (UCD; n ¼ 13). The percentage of fat in the diet was calculated from the nutritional information available for each product and the amount in grams consumed by the animals.…”

Section: Animalsmentioning

confidence: 99%

Undernutrition during suckling in rats elevates plasma adiponectin and its receptor in skeletal muscle regardless of diet composition: a protective effect?

et al. 2008

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Objective: Nutrition during critical periods in early life may increase the subsequent risk of obesity, hypertension and metabolic diseases in adulthood. Few studies have focused on the long-term consequences of poor nutrition during the suckling period on the susceptibility to developing obesity when exposed to a palatable cafeteria-style high-fat diet (CD) after weaning. Design: This study examined the impact of early undernutrition, followed by CD exposure, on blood pressure, hormones and genes important for insulin sensitivity and metabolism and skeletal muscle mRNA expression of adiponectin receptor 1 (AdipoR1), carnitine palmitoyl-transferase I (CPT-1), cytochrome c oxidase 4 (COX4) and peroxisome proliferator-activated receptor a (PPARa). Following normal gestation, Sprague-Dawley rat litters were adjusted to 18 (undernourished) or 12 (control) pups. Rats were weaned (day 21) onto either palatable CD or standard chow. Results: Early undernourished rats were significantly lighter than control by 17 days, persisting into adulthood only when animals were fed chow after weaning. Regardless of litter size, rats fed CD had doubled fat mass at 15 weeks of age, and significant elevations in plasma leptin, insulin and adiponectin. Importantly, undernutrition confined to the suckling period, elevated circulating adiponectin regardless of post-weaning diet. Blood pressure was reduced in early undernourished rats fed chow, and increased by CD. Early undernutrition was associated with long-term elevations in the expression of AdipoR1, CPT-1, COX4 and PPARa in skeletal muscle. Conclusion: This study demonstrates the important role of early nutrition on body weight and metabolism, suggesting early undernourishment enhances insulin sensitivity and fatty-acid oxidation. The long-term potential benefit of limiting nutrition in the early postnatal period warrants further investigation.

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Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet

Cited by 45 publications

References 67 publications

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

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

Established maternal obesity in the rat reprograms hypothalamic appetite regulators and leptin signaling at birth

Undernutrition during suckling in rats elevates plasma adiponectin and its receptor in skeletal muscle regardless of diet composition: a protective effect?

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