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Czyzyk T.A.,Obesity Research | Nogueiras R.,University of Cincinnati | Nogueiras R.,University of Santiago de Compostela | Lockwood J.F.,Obesity Research | And 6 more authors.
FASEB Journal | Year: 2010

General opioid receptor antagonists reduce food intake and body weight in rodents, but the contributions of specific receptor subtypes are unknown. We examined whether genetic deletion of the κ-opioid receptor (KOR) in mice alters metabolic physiology. KOR-knockout (KO) and wild-type (WT) mice were fed a high-energy diet (HED) for 16 wk. KO mice had 28% lower body weight and 45% lower fat mass when compared to WT mice fed an HED. No differences in caloric intake were found. An HED reduced energy expenditure in WT mice, but not in KO mice. KOR deficiency led to an attenuation of triglyceride synthesis in the liver. Malonyl CoA levels were also reduced in response to an HED, thereby promoting hepatic β-oxidation. Glycemic control was also found to be improved in KO mice. These data suggest a key role for KORs in the central nervous system regulation of the metabolic adaptation to an HED, as we were unable to detect expression of KOR in liver, white adipose tissue, or skeletal muscle in WT mice. This study provides the first evidence that KORs play an essential physiological role in the control of hepatic lipid metabolism, and KOR activation is a permissive signal toward fat storage. © FASEB. Source


News Article | January 11, 2016
Site: http://boingboing.net

Why all scientific diet research turns out to be bullshit The gold standard for researching the effects of diet on health is the self-reported food-diary, which is prone to lots of error, underreporting of "bad" food, and changes in diet that result from simply keeping track of what you're eating. The standard tool for correcting these errors comparisons with more self-reported tests. As if that wasn't bad enough, eating correlates with everything, so if you go "p-hacking" through the data, looking for correlations after the fact. My take on all this is that if there was a gross, easily observable effect from eating food that humans have been eating for hundreds or thousands of years, we'd already know about it. That's why the amazing study showing that kiwi fruit promote good sleep turns out to have only 24 subjects, only two of them men, to rely on self-reporting, and to be funded by the kiwi industry. That's why the incredible news that tomatoes improve memory turns out to be a preliminary result of a small study on very old Japanese people. If you're not very old and of Japanese descent, that finding means something between nothing and so little as to be indistinguishable from nothing. So a good rule of thumb, as far as I'm concerned, is that any nutrition study that finds any genuinely surprising, large-scale effect, is bullshit. Tiny, difficult-to-disentangle effects? Sure, there's probably a lot of those. But "Eating peanuts makes you grow extra nipples on your ass-cheeks?" If that were the case, we'd have noticed by now. Although concerns about self-reported dietary intakes have been around for decades, the debate has come to a head in recent years, said David Allison, director of the University of Alabama’s Nutrition Obesity Research Center in Birmingham. Allison was an author of a 2014 expert report from the Energy Balance Measurement Working Group that called it “unacceptable” to use “decidedly inaccurate” methods of measurement to set health care policies, research and clinical practice. “In this case,” the researchers wrote, “the adage ‘something is better than nothing’ must be changed to ‘something is worse than nothing.’” The problems with food questionnaires go even deeper. They aren’t just unreliable, they also produce huge data sets with many, many variables. The resulting cornucopia of possible variable combinations makes it easy to p-hack your way to sexy (and false) results, as we learned when we invited readers to take an FFQ and answer a few other questions about themselves. We ended up with 54 complete responses and then looked for associations — much as researchers look for links between foods and dreaded diseases. It was silly easy to find them. You Can’t Trust What You Read About Nutrition [Christie Aschwanden/538]


Czyzyk T.A.,Obesity Research | Romero-Pico A.,University of Santiago de Compostela | Pintar J.,Johnson University | McKinzie J.H.,Obesity Research | And 3 more authors.
FASEB Journal | Year: 2012

Pharmacological manipulation of opioid receptors alters feeding behavior. However, the individual contributions of each opioid receptor subtype on energy balance remain largely unknown. Herein, we investigated whether genetic disruption of the δ-opioid receptor (DOR) also controls energy homeostasis. Mice lacking DOR and wild-type mice were fed with standard diet and high-energy diet (HED). Mice were analyzed in vivo with the indirect calorimetry system, and tissues were analyzed by real-time PCR and Western blot analysis. DOR-knockout (KO) mice gained less weight (P<0.01) and had lower fat mass (P<0.01) when compared to WT mice fed an HED. Although DOR-KO mice were hyperphagic, they showed higher energy expenditure (P<0.05), which was the result of an increased activation of the thermogenic program in brown adipose tissue. The increased nonshivering thermogenesis involved the stimulation of uncoupling protein 1 (UCP1; P<0.01), peroxisome proliferator-activated receptor γ coactivator (PGC1α; P<0.05), and fibroblast growth factor 21 (FGF21; P<0.01). DOR deficiency also led to an attenuation of triglyceride content in the liver (P<0.05) in response to an HED. These findings reveal a novel role of DOR in the control of thermogenic markers and energy expenditure, and they provide a potential new therapeutic approach for the treatment of obesity. © FASEB. Source


Czyzyk T.A.,Obesity Research | Sahr A.E.,Obesity Research | Statnick M.A.,Obesity Research
Obesity | Year: 2010

Binge eating disorder (BED) is characterized by excessive food intake during a short period of time and is often associated with obesity. Mouse models of binge-like eating behavior are lacking making it difficult to employ genetic models in the identification of mechanisms regulating excessive eating. We report a rapid and simple model to induce binge-like eating behavior in mice that does not require food deprivation or exogenous stressors. Weekly 24h access to a nutritionally complete high energy diet (HED), along with continuous access to standard chow, resulted in a significant increase in HED intake following its presentation compared to mice that had continuous access to both diets. Mice exhibiting binge-like eating consumed one-third of their normal total daily caloric intake within 2.5h of HED presentation. Moreover, total 24-h caloric intakes were increased by 50% in mice exhibiting binge-like eating. Following repeated cycles, binge-like eating of the HED was maintained over several weeks with no evidence of habituation or significant alterations in body weight and adiposity. Pharmacological evaluation of binge-like eating behavior was performed using clinically employed compounds. Interestingly, binge-like eating was dose-dependently decreased by fluoxetine, but not baclofen or topiramate. These data support clinical validation of this mouse model of binge-like eating behavior, as fluoxetine has been shown to reduce binge frequency in human subjects with BED. The availability of transgenic and knockout mice will allow for the determination of genes that are involved in the initiation and maintenance of binge-like eating behavior. © 2009 The Obesity Society. Source

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