Browsing by Subject "FOOD-INTAKE"

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  • Thorgeirsson, T. E.; Gudbjartsson, D. F.; Sulem, P.; Besenbacher, S.; Styrkarsdottir, U.; Thorleifsson, G.; Walters, G. B.; Furberg, H.; Sullivan, P. F.; Marchini, J.; McCarthy, M. I.; Steinthorsdottir, V.; Thorsteinsdottir, U.; Stefansson, K.; TAG Consortium; Oxford-GSK Consortium; ENGAGE Consortium; Kaprio, Jaakko; Tuomilehto, Jaakko; Shen, Huei-Yi (2013)
  • Pashay Ahi, Ehsan; Duenser, Anna; Singh, Pooja; Gessl, Wolfgang; Sturmbauer, Christian (2020)
    Feeding is a complex behaviour comprised of satiety control, foraging, ingestion and subsequent digestion. Cichlids from the East African Great Lakes are renowned for their diverse trophic specializations, largely predicated on highly variable jaw morphologies. Thus, most research has focused on dissecting the genetic, morphological and regulatory basis of jaw and teeth development in these species. Here for the first time we explore another aspect of feeding, the regulation of appetite related genes that are expressed in the brain and control satiety in cichlid fishes. Using qPCR analysis, we first validate stably expressed reference genes in the brain of six haplochromine cichlid species at the end of larval development prior to foraging. We next evaluate the expression of 16 appetite related genes in herbivorous and carnivorous species from the parallel radiations of Lake Tanganyika, Malawi and Victoria. Interestingly, we find increased expression of two appetite-regulating genes (anorodgenic genes), cart and npy2r, in the brain of carnivorous species in all the three lakes. This supports the notion that appetite gene regulation might play a part in determining trophic niche specialization in divergent cichlid species, already prior to exposure to different diets. Our study contributes to the limited body of knowledge on the neurological circuitry that controls feeding transitions and adaptations in cichlids and other teleosts.
  • McFarlane, S. Eryn; Ålund, Murielle; Sirkiä, Päivi M.; Qvarnström, Anna (2018)
    Variation in relative fitness of competing recently formed species across heterogeneous environments promotes coexistence. However, the physiological traits mediating such variation in relative fitness have rarely been identified. Resting metabolic rate (RMR) is tightly associated with life history strategies, thermoregulation, diet use, and inhabited latitude and could therefore moderate differences in fitness responses to fluctuations in local environments, particularly when species have adapted to different climates in allopatry. We work in a long-term study of collared (Ficedula albicollis) and pied flycatchers (Ficedula hypoleuca) in a recent hybrid zone located on the Swedish island of Oland in the Baltic Sea. Here, we explore whether differences in RMR match changes in relative performance of growing flycatcher nestlings across environmental conditions using an experimental approach. The fitness of pied flycatchers has previously been shown to be less sensitive to the mismatch between the peak in food abundance and nestling growth among late breeders. Here, we find that pied flycatcher nestlings have lower RMR in response to higher ambient temperatures (associated with low food availability). We also find that experimentally relaxed nestling competition is associated with an increased RMR in this species. In contrast, collared flycatcher nestlings did not vary their RMR in response to these environmental factors. Our results suggest that a more flexible nestling RMR in pied flycatchers is responsible for the better adaptation of pied flycatchers to the typical seasonal changes in food availability experienced in this hybrid zone. Generally, subtle physiological differences that have evolved when species were in allopatry may play an important role to patterns of competition, coexistence, or displacements between closely related species in secondary contact.
  • Graff, Mariaelisa; Scott, Robert A.; Justice, Anne E.; Young, Kristin L.; Feitosa, Mary F.; Barata, Llilda; Winkler, Thomas W.; Chu, Audrey Y.; Mahajan, Anubha; Hadley, David; Xue, Luting; Workalemahu, Tsegaselassie; Heard-Costa, Nancy L.; den Hoed, Marcel; Ahluwalia, Tarunveer S.; Qi, Qibin; Ngwa, Julius S.; Renstrom, Frida; Quaye, Lydia; Eicher, John D.; Hayes, James E.; Cornelis, Marilyn; Kutalik, Zoltan; Lim, Elise; Luan, Jian'an; Huffman, Jennifer E.; Zhang, Weihua; Zhao, Wei; Griffin, Paula J.; Haller, Toomas; Ahmad, Shafqat; Marques-Vidal, Pedro M.; Bien, Stephanie; Yengo, Loic; Teumer, Alexander; Smith, Albert Vernon; Kumari, Meena; Harder, Marie Neergaard; Justesen, Johanne Marie; Kleber, Marcus E.; Hollensted, Mette; Lohman, Kurt; Rivera, Natalia V.; Whitfield, John B.; Kristiansson, Kati; Havulinna, Aki S.; Koistinen, Heikki A.; Perola, Markus; Tuomilehto, Jaakko; Kivimaki, Mika; CHARGE Consortium; EPIC-InterAct Consortium; PAGE Consortium (2017)
    Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by similar to 30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.
  • Grönberg, Malin; Nilsson, Cecilia; Markholm, Ida; Hedenfalk, Ingrid; Blomqvist, Carl; Holmberg, Lars; Tiensuu Janson, Eva; Fjällskog, Marie-Louise (2018)
    Ghrelin and obestatin are two gastrointestinal peptides, derived from a common precursor. Expression of both peptides have been found in breast cancer tissue and ghrelin has been associated with breast cancer development. Ghrelin expression is associated with longer survival in women diagnosed with invasive and node negative breast cancer. The clinical implications of the peptide expression in male breast cancer are unclear. The aim of this study was to investigate the role and potential clinical value of ghrelin and obestatin in male breast cancer. A tissue microarray of invasive male breast cancer specimens from 197 patients was immunostained with antibodies versus the two peptides. The expression of the peptides was correlated to previously known prognostic factors in breast cancer and to the outcome. No strong correlations were found between ghrelin or obestatin expression and other known prognostic factors. Only ghrelin expression was statistically significantly correlated to breast cancer-specific survival (HR 0.39, 95% CI 0.18-0.83) in univariate analyses and in multivariate models, adjusted for tumor size and node status (HR 0.38, 95% CI 0.17-0.87). HR for obestatin was 0.38 (95% CI 0.11-1.24). Ghrelin is a potential prognostic factor for breast cancer death in male breast cancer. Patients with tumors expressing ghrelin have a 2.5-fold lower risk for breast cancer death than those lacking ghrelin expression. Drugs targeting ghrelin are currently being investigated in clinical studies treating metabolic or nutritional disorders. Ghrelin should be further evaluated in forthcoming studies as a prognostic marker with the aim to be included in decision algorithms.
  • Jarvela-Reijonen, Elina; Karhunen, Leila; Sairanen, Essi; Rantala, Sanni; Laitinen, Jaana; Puttonen, Sampsa; Peuhkuri, Katri; Hallikainen, Maarit; Juvonen, Kristiina; Myllymaki, Tero; Fohr, Tiina; Pihlajamaki, Jussi; Korpela, Riitta; Ermes, Miikka; Lappalainen, Raimo; Kolehmainen, Marjukka (2016)
    Stress-related eating may be a potential factor in the obesity epidemic. Rather little is known about how stress associates with eating behavior and food intake in overweight individuals in a free-living situation. Thus, the present study aims to investigate this question in psychologically distressed overweight and obese working-aged Finns. The study is a cross-sectional baseline analysis of a randomized controlled trial. Of the 339 study participants, those with all the needed data available (n = 297, 84% females) were included. The mean age was 48.9 y (SD = 7.6) and mean body mass index 31.3 kg/m(2) (SD = 3.0). Perceived stress and eating behavior were assessed by self-reported questionnaires Perceived Stress Scale (PSS), Intuitive Eating Scale, the Three-Factor Eating Questionnaire, Health and Taste Attitude Scales and ecSatter Inventory. Diet and alcohol consumption were assessed by 48-h dietary recall, Index of Diet Quality, and AUDIT-C. Individuals reporting most perceived stress (i.e. in the highest PSS tertile) had less intuitive eating, more uncontrolled eating, and more emotional eating compared to those reporting less perceived stress (p <0.05). Moreover, individuals in the highest PSS tertile reported less cognitive restraint and less eating competence than those in the lowest tertile (p <0.05). Intake of whole grain products was the lowest among those in the highest PSS tertile (p <0.05). Otherwise the quality of diet and alcohol consumption did not differ among the PSS tertiles. In conclusion, high perceived stress was associated with the features of eating behavior that could in turn contribute to difficulties in weight management. Stress-related way of eating could thus form a potential risk factor for obesity. More research is needed to develop efficient methods for clinicians to assist in handling stress-related eating in the treatment of obese people. (C) 2016 Elsevier Ltd. All rights reserved.
  • Heikelä, Hanna; Ruohonen, Suvi T.; Adam, Marion; Viitanen, Riikka; Liljenback, Heidi; Eskola, Olli; Gabriel, Michael; Mairinoja, Laura; Pessia, Alberto; Velagapudi, Vidya; Roivainen, Anne; Zhang, Fu-Ping; Strauss, Leena; Poutanen, Matti (2020)
    Hydroxysteroid 17-beta dehydrogenase 12 (HSD17B12) is suggested to be involved in the elongation of very long chain fatty acids. Previously, we have shown a pivotal role for the enzyme during mouse development. In the present study we generated a conditional Hsd17b12 knockout (HSD17B12cKO) mouse model by breeding mice homozygous for a floxed Hsd17b12 allele with mice expressing the tamoxifen-inducible Cre recombinase at the ROSA26 locus. Gene inactivation was induced by administering tamoxifen to adult mice. The gene inactivation led to a 20% loss of body weight within six days, associated with drastic reduction in both white (83% males, 75% females) and brown (65% males, 60% females) fat, likely due to markedly reduced food and water intake. Furthermore, the knockout mice showed sickness behavior and signs of liver toxicity, specifically microvesicular hepatic steatosis and increased serum alanine aminotransferase (4.6-fold in males, 7.7-fold in females). The hepatic changes were more pronounced in females than males. Pro-inflammatory cytokines, such as interleukin 6 (IL-6), IL-17 and granulocyte-colony stimulating factor were increased in the HSD17B12cKO mice indicating inflammatory response. Serum lipidomics study showed an increase in the amount of dihydroceramides, despite the dramatic overall loss of lipids. In line with the proposed role for HSD17B12 in the fatty acid elongation, we observed accumulation of ceramides, dihydroceramides, hexosylceramides and lactosylceramides with shorter than 18-carbon fatty acid side chains in the serum. The results indicate that HSD17B12 is essential for proper lipid homeostasis, and HSD17B12 deficiency rapidly results in fatal systemic inflammation and lipolysis in adult mice.
  • Viljakainen, Jannina; Raju, Sajan C.; Viljakainen, Heli; Figueiredo, Rejane Augusta de Oliveira; Roos, Eva; Weiderpass, Elisabete; Rounge, Trine B. (2020)
    Background Diet may influence health directly or indirectly via the human microbiota, emphasizing the need to unravel these complex relationships for future health benefits. Associations between eating habits and gut microbiota have been shown, but less is known about the association between eating habits and saliva microbiota. Objective The aim of this study was to investigate if eating habits and meal patterns are associated with the saliva microbiota. Methods In total, 842 adolescents, aged 11-14 years, from the Finnish Health in Teens (Fin-HIT) study cohort were included in this study. Eating habits and breakfast and dinner patterns were derived from a web-based questionnaire answered in school. Three major eating habit groups were identified: fruit and vegetable avoiders (FV avoiders), healthy and unhealthy. Microbiota profiles were produced from 16S rRNA gene (V3-V4) sequencing of DNA from the saliva samples. Statistical models were adjusted for gender, age, parental language, body mass index (BMI) categories, and sequencing depth. Results Regular breakfast eaters had a higher alpha diversity (Shannon index with mean (standard error of means) 2.27 (0.03) vs. 2.22 (0.03), p = 0.06, inverse Simpson's index with 6.27 (0.17) vs. 5.80 (0.02), p = 0.01), and slight differences in bacterial composition (PERMANOVA: p = 0.001) compared with irregular breakfast eaters. A similar trend in alpha diversity was observed between regular and irregular dinner eaters (Shannon index with 2.27 (0.03) vs. 2.22 (0.03), p = 0.054, inverse Simpson's index with 6.23 (0.17) vs. 6.04 (0.22), p = 0.28), while no difference was found in composition (PERMANOVA: p = 0.08). No differences were identified between eating habit groups and saliva microbiota diversity (Shannon index p = 0.77, inverse Simpson's index p = 0.94) or composition (PERMANOVA: p = 0.13). FV avoiders, irregular breakfast eaters and irregular dinner eaters had high abundances of Prevotella. Conclusion Regularity of eating, especially breakfast eating, was associated with more diverse saliva microbiota and different composition compared with irregular eaters. However, the dissimilarities in composition were small between regular and irregular breakfast eaters. Our results suggest that Prevotella abundances in saliva were common in FV avoiders and meal skippers. However, the clinical implications of these findings need to be evaluated in future studies.
  • Silventoinen, Karri; Konttinen, Hanna (2020)
    Obesity has dramatically increased during the last decades and is currently one of the most serious global health problems. We present a hypothesis that obesity is a neuro-behavioral disease having a strong genetic background mediated largely by eating behavior and is sensitive to the macro-environment; we study this hypothesis from the perspective of genetic research. Genetic family and genome-wide-association studies have shown well that body mass index (BMI, kg/m(2)) is a highly heritable and polygenic trait. New genetic variation of BMI emerges after early childhood. Candidate genes of BMI notably express in brain tissue, supporting that this new variation is related to behavior. Obesogenic environments at both childhood family and societal levels reinforce the genetic susceptibility to obesity. Genetic factors have a clear influence on macro-nutrient intake and appetite-related eating behavior traits. Results on the gene-by-diet interactions in obesity are mixed, but emerging evidence suggests that eating behavior traits partly mediate the effect of genes on BMI. However, more rigorous prospective study designs controlling for measurement bias are still needed.
  • Sieminski, Mariusz; Szypenbejl, Jacek; Partinen, Eemil (2018)
    The aim of this review was to summarize collected data on the role of orexin and orexin neurons in the control of sleep and blood pressure. Although orexins (hypocretins) have been known for only 20 years, an impressive amount of data is now available regarding their physiological role. Hypothalamic orexin neurons are responsible for the control of food intake and energy expenditure, motivation, circadian rhythm of sleep and wake, memory, cognitive functions, and the cardiovascular system. Multiple studies show that orexinergic stimulation results in increased blood pressure and heart rate and that this effect may be efficiently attenuated by orexinergic antagonism. Increased activity of orexinergic neurons is also observed in animal models of hypertension. Pharmacological intervention in the orexinergic system is now one of the therapeutic possibilities in insomnia. Although the role of orexin in the control of blood pressure is well described, we are still lacking clinical evidence that this is a possibility for a new approach in the treatment of cardiovascular diseases.
  • Thompson, Miles D.; Xhaard, Henri; Sakurai, Takeshi; Rainero, Innocenzo; Kukkonen, Jyrki P. (2014)
    Orexin/hypocretin peptide mutations are rare in humans. Even though human narcolepsy is associated with orexin deficiency, this is only extremely rarely due to mutations in the gene coding prepro-orexin, the precursor for both orexin peptides. In contrast, coding and non-coding variants of the OX1 and OX2 orexin receptors have been identified in many human populations; sometimes, these have been associated with disease phenotype, although most confer a relatively low risk. In most cases, these studies have been based on a candidate gene hypothesis that predicts the involvement of orexins in the relevant pathophysiological processes. In the current review, the known human OX1/HCRTR1 and OX2/HCRTR2 genetic variants/polymorphisms as well as studies concerning their involvement in disorders such as narcolepsy, excessive daytime sleepiness, cluster headache, polydipsia-hyponatremia in schizophrenia, and affective disorders are discussed. In most cases, the functional cellular or pharmacological correlates of orexin variants have not been investigated-with the exception of the possible impact of an amino acid 10 Pro/Ser variant of OX2 on orexin potency-leaving conclusions on the nature of the receptor variant effects speculative. Nevertheless, we present perspectives that could shape the basis for further studies. The pharmacology and other properties of the orexin receptor variants are discussed in the context of GPCR signaling. Since orexinergic therapeutics are emerging, the impact of receptor variants on the affinity or potency of ligands deserves consideration. This perspective (pharmacogenetics) is also discussed in the review.
  • Silventoinen, Karri; Jelenkovic, Aline; Latvala, Antti; Yokoyama, Yoshie; Sund, Reijo; Sugawara, Masumi; Tanaka, Mami; Matsumoto, Satoko; Aaltonen, Sari; Piirtola, Maarit; Freitas, Duarte L.; Maia, Jose A.; Oncel, Sevgi Y.; Aliev, Fazil; Ji, Fuling; Ning, Feng; Pang, Zengchang; Rebato, Esther; Saudino, Kimberly J.; Cutler, Tessa L.; Hopper, John L.; Ullemar, Vilhelmina; Almqvist, Catarina; Magnusson, Patrik K. E.; Cozen, Wendy; Hwang, Amie E.; Mack, Thomas M.; Willemsen, Gonneke; Bartels, Meike; van Beijsterveldt, Catharina E. M.; Nelson, Tracy L.; Whitfield, Keith E.; Sung, Joohon; Kim, Jina; Lee, Jooyeon; Lee, Sooji; Llewellyn, Clare H.; Fisher, Abigail; Medda, Emanuela; Nistico, Lorenza; Toccaceli, Virgilia; Baker, Laura A.; Tuvblad, Catherine; Corley, Robin P.; Huibregtse, Brooke M.; Derom, Catherine A.; Vlietinck, Robert F.; Loos, Ruth J. F.; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; Burt, S. Alexandra; Klump, Kelly L.; Silberg, Judy L.; Maes, Hermine H.; Krueger, Robert F.; McGue, Matt; Pahlen, Shandell; Gatz, Margaret; Butler, David A.; Harris, Jennifer R.; Nilsen, Thomas S.; Harden, K. Paige; Tucker-Drob, Elliot M.; Franz, Carol E.; Kremen, William S.; Lyons, Michael J.; Lichtenstein, Paul; Jeong, Hoe-Uk; Hur, Yoon-Mi; Boomsma, Dorret I.; Sorensen, Thorkild I. A.; Kaprio, Jaakko (2019)
    Objective The objective of this study was to analyze how parental education modifies the genetic and environmental variances of BMI from infancy to old age in three geographic-cultural regions. Methods A pooled sample of 29 cohorts including 143,499 twin individuals with information on parental education and BMI from age 1 to 79 years (299,201 BMI measures) was analyzed by genetic twin modeling. Results Until 4 years of age, parental education was not consistently associated with BMI. Thereafter, higher parental education level was associated with lower BMI in males and females. Total and additive genetic variances of BMI were smaller in the offspring of highly educated parents than in those whose parents had low education levels. Especially in North American and Australian children, environmental factors shared by co-twins also contributed to the higher BMI variation in the low education level category. In Europe and East Asia, the associations of parental education with mean BMI and BMI variance were weaker than in North America and Australia. Conclusions Lower parental education level is associated with higher mean BMI and larger genetic variance of BMI after early childhood, especially in the obesogenic macro-environment. The interplay among genetic predisposition, childhood social environment, and macro-social context is important for socioeconomic differences in BMI.
  • Matricciani, Lisa; Bin, Yu Sun; Lallukka, Tea; Kronholm, Erkki; Dumuid, Dorothea; Paquet, Catherine; Olds, Tim (2017)
    Sleep is important for the physical, social and mental well-being of both children and adults. Over the years, there has been a general presumption that sleep will inevitably decline with the increase in technology and a busy 24-hour modern lifestyle. This narrative review discusses the empirical evidence for secular trends in sleep duration and the implications of these trends. (c) 2017 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.
  • Karvinen, Sira; Waller, Katja; Silvennoinen, Mika; Koch, Lauren G.; Britton, Steven L.; Kaprio, Jaakko; Kainulainen, Heikki; Kujala, Urho M. (2015)
    Observational studies report a strong inverse relationship between leisure-time physical activity and all-cause mortality. Despite suggestive evidence from population-based associations, scientists have not been able to show a beneficial effect of physical activity on the risk of death in controlled intervention studies among individuals who have been healthy at baseline. On the other hand, high cardiorespiratory fitness is known to be a strong predictor of reduced mortality, even more robust than physical activity level itself. Here, in both animals and/or human twins, we show that the same genetic factors influence physical activity levels, cardiorespiratory fitness, and risk of death. Previous observational follow-up studies in humans suggest that increasing fitness through physical activity levels could prolong life; however, our controlled interventional study with laboratory rats bred for low and high intrinsic fitness contrast with these findings. Also, we find no evidence for the suggested association using pairwise analysis among monozygotic twin pairs who are discordant in their physical activity levels. Based on both our animal and human findings, we propose that genetic pleiotropy might partly explain the frequently observed associations between high baseline physical activity and later reduced mortality in humans.
  • UK10K Consortium; Yang, Yongjie; van der Klaauw, Agatha A.; Lonnqvist, Jouko; Palotie, Aarno; Paunio, Tiina; Pietilainen, Olli; Suvisaari, Jaana (2019)
    Hypothalamic neurons expressing the anorectic peptide Pro-opiomelanocortin (Pomc) regulate food intake and body weight. Here, we show that Steroid Receptor Coactivator-1 (SRC-1) interacts with a target of leptin receptor activation, phosphorylated STAT3, to potentiate Pomc transcription. Deletion of SRC-1 in Pomc neurons in mice attenuates their depolarization by leptin, decreases Pomc expression and increases food intake leading to high-fat diet-induced obesity. In humans, fifteen rare heterozygous variants in SRC-1 found in severely obese individuals impair leptin-mediated Pomc reporter activity in cells, whilst four variants found in non-obese controls do not. In a knock-in mouse model of a loss of function human variant (SRC-1L1376P), leptin-induced depolarization of Pomc neurons and Pomc expression are significantly reduced, and food intake and body weight are increased. In summary, we demonstrate that SRC-1 modulates the function of hypothalamic Pomc neurons, and suggest that targeting SRC-1 may represent a useful therapeutic strategy for weight loss.
  • Lipsanen, Jari; Elovainio, Marko; Hakulinen, Christian; Tremblay, Mark S.; Rovio, Suvi; Lagström, Hanna; Jaakkola, Johanna M.; Jula, Antti; Rönnemaa, Tapani; Viikari, Jorma; Niinikoski, Harri; Simell, Olli; Raitakari, Olli T.; Pahkala, Katja; Pulkki-Råback, Laura (2020)
    Background and objectives: Temperament may be associated with eating behaviors over the lifespan. This study examined the association of toddlerhood temperament with dietary behavior and dietary intervention outcomes across 18 years. Methods: The study comprised 660 children (52% boys) from The Special Turku Intervention Project (STRIP), which is a longitudinal randomized controlled trial from the age of 7 months until the age of 20 years (1990-2010). Temperament was assessed using Carey temperament scales when the participants were 2 years of age. Latent profile analysis yielded three temperament groups, which were called negative/low regulation (19% of the children), neutral/average regulation (52%) and positive/high regulation (28%). Dietary behavior was examined from 2 to 20 years of age using food records, which were converted into a diet score (mean= 15.7, SD 4.6). Mixed random-intercept growth curve analysis was the main analytic method. Results: Dietary behavior showed a significant quadratic U-shaped curve over time (B for quadratic association = 0.39, P<.001; B for linear association = 0.09, P = 0.58). Children in the negative/low regulation temperament group had a lower diet score (less healthy diet) across the 18 years compared to children in the neutral/average or in the positive/high regulation group. Temperament was not associated with the rate of change in diet over time. Temperament did not have any interactive effects with the intervention (F [2, 627], P = 0.72). Conclusion: Children with a temperament profile characterized by high negative mood, high irregularity and high intensity in emotion expression constitute a risk group for less healthy eating over the lifespan.
  • Huseinovic, Ena; Winkvist, Anna; Freisling, Heinz; Slimani, Nadia; Boeing, Heiner; Buckland, Genevieve; Schwingshackl, Lukas; Olsen, Anja; Tionneland, Anne; Stepien, Magdalena; Boutron-Ruault, Marie-Christine; Mancini, Francesca; Artaud, Fanny; Kuehn, Tilman; Katzke, Verena; Trichopoulou, Antonia; Naska, Androniki; Orfanos, Philippos; Tumino, Rosario; Masala, Giovanna; Krogh, Vittorio; de Magistris, Maria Santucci; Ocke, Marga C.; Brustad, Magritt; Jensen, Torill Enget; Skeie, Guri; Rodriguez-Barranco, Miguel; Maria Huerta, Jose; Ardanaz, Eva; Ramon Quiros, Jose; Jakszyn, Paula; Sonestedt, Emily; Ericson, Ulrika; Wennberg, Maria; Key, Timothy J.; Aune, Dagfinn; Riboli, Elio; Weiderpass, Elisabete; Forslund, Helene Berteus (2019)
    Objective To examine timing of eating across ten European countries. Design Cross-sectional analysis of the European Prospective Investigation into Cancer and Nutrition (EPIC) calibration study using standardized 24 h diet recalls collected during 1995-2000. Eleven predefined food consumption occasions were assessed during the recall interview. We present time of consumption of meals and snacks as well as the later:earlier energy intake ratio, with earlier and later intakes defined as 06.00-14.00 and 15.00-24.00 hours, respectively. Type III tests were used to examine associations of sociodemographic, lifestyle and health variables with timing of energy intake. Setting Ten Western European countries. Subjects In total, 22 985 women and 13 035 men aged 35-74 years (n 36 020). Results A south-north gradient was observed for timing of eating, with later consumption of meals and snacks in Mediterranean countries compared with Central and Northern European countries. However, the energy load was reversed, with the later:earlier energy intake ratio ranging from 0 center dot 68 (France) to 1 center dot 39 (Norway) among women, and from 0 center dot 71 (Greece) to 1 center dot 35 (the Netherlands) among men. Among women, country, age, education, marital status, smoking, day of recall and season were all independently associated with timing of energy intake (all P
  • Houlahan, Kathleen E.; Prokopec, Stephenie D.; Moffat, Ivy D.; Lindén, Jere; Lensu, Sanna; Okey, Allan B.; Pohjanvirta, Raimo; Boutros, Paul C. (2015)
    In some mammals, halogenated aromatic hydrocarbon (HAH) exposure causes wasting syndrome, defined as significant weight loss associated with lethal outcomes. The most potent HAH in causing wasting is 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD), which exerts its toxic effects through the aryl hydrocarbon receptor (AHR). Since TCDD toxicity is thought to predominantly arise from dysregulation of AHR-transcribed genes, it was hypothesized that wasting syndrome is a result of to TCDD-induced dysregulation of genes involved in regulation of food-intake. As the hypothalamus is the central nervous systems' regulatory center for food-intake and energy balance. Therefore, mRNA abundances in hypothalamic tissue from two rat strains with widely differing sensitivities to TCDD-induced wasting syndrome: TCDD-sensitive Long-Evans rats and TCDD-resistant Han/Wistar rats, 23 h after exposure to TCDD (100 mu g/kg) or corn oil vehicle. TCDD exposure caused minimal transcriptional dysregulation in the hypothalamus, with only 6 genes significantly altered in Long-Evans rats and 15 genes in Han/Wistar rats. Two of the most dysregulated genes were Cyp1a1 and Nqo1, which are induced by TCDD across a wide range of tissues and are considered sensitive markers of TCDD exposure. The minimal response of the hypothalamic transcriptome to a lethal dose of TCDD at an early time-point suggests that the hypothalamus is not the predominant site of initial events leading to hypophagia and associated wasting. TCDD may affect feeding behaviour via events upstream or downstream of the hypothalamus, and further work is required to evaluate this at the level of individual hypothalamic nuclei and subregions. (C) 2014 The Authors. Published by Elsevier Ireland Ltd.