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Objectives The Three-Factor-Eating Questionnaire (TFEQ) is an established instrument to assess eating behavior in terms of dietary restraint, disinhibition and hunger. Methods The aims of this study were to examine (1) the correlation between eating behavior and body mass index (BMI), (2) the correlation between eating behavior and masticatory performance in terms of bite size and eating speed, and (3) the effects of gender on these correlations in 56 healthy subjects (33 males [21.9 ± 2.8 years old] and 23 females [21.7 ± 2.2 years old]). Results We found a significant correlation between restraint and BMI only in females and between hunger and BMI only in males. However, disinhibition and BMI were significantly correlated in both males and females. We also found a significant correlation between bite size and hunger only in males and between eating speed and disinhibition in both males and females. Conclusions These findings underline the importance of gender-specific counselling and behavioral treatment of obesity.

Tooth loss or incorrect positioning causes occlusal disharmony. Furthermore, tooth loss and atrial fibrillation (AF) are both risk factors for ischemic stroke and coronary heart disease. Therefore, we hypothesized that occlusal disharmony-induced stress increases susceptibility to AF, and we designed the present study to test this idea in mice. Bite-opening (BO) was done by cementing a suitable appliance onto the mandibular incisor to cause occlusal disharmony by increasing the vertical height of occlusion by 0.7 mm for a period of 2 weeks. AF susceptibility, evaluated in terms of the duration of AF induced by transesophageal burst pacing, was significantly increased concomitantly with atrial remodeling, including fibrosis, myocyte apoptosis and oxidative DNA damage, in BO mice. The BO-induced atrial remodeling was associated with increased calmodulin kinase II-mediated ryanodine receptor 2 phosphorylation on serine 2814, as well as inhibition of Akt phosphorylation. However, co-treatment with propranolol, a non-selective β-blocker, ameliorated these changes in BO mice. These data suggest that improvement of occlusal disharmony by means of orthodontic treatment might be helpful in the treatment or prevention of AF.

The G protein-regulated inducer of neurite growth (GRIN) family has three isoforms (GRIN1-3), which bind to the Gαi/o subfamily of G protein that mediate signal processing via G protein-coupled receptors (GPCRs). Here, we show that GRIN3 is involved in regulation of dopamine-dependent behaviors and is essential for activation of the dopamine receptors (DAR)-β-arrestin signaling cascade. Analysis of functional regions of GRIN3 showed that a di-cysteine motif (Cys751/752) is required for plasma membrane localization. GRIN3 was co-immunoprecipitated with GPCR kinases 2/6 and β-arrestins 1/2. Among GRINs, only GRIN3, which is highly expressed in striatum, strongly interacted with β-arrestin 2. We also generated GRIN3-knockout mice (GRIN3KO). GRIN3KO exhibited reduced locomotor activity and increased anxiety-like behavior in the elevated maze test, as well as a reduced locomoter response to dopamine stimulation. We also examined the phosphorylation of Akt at threonine 308 (phospho308-Akt), which is dephosphorylated via a β-arrestin 2-mediated pathway. Dephosphorylation of phospho308-Akt via the D2R-β-arrestin 2 signaling pathway was completely abolished in striatum of GRIN3KO. Our results suggest that GRIN3 has a role in recruitment and assembly of proteins involved in β-arrestin-dependent, G protein-independent signaling.

Occlusal disharmony leads to morphological changes in the hippocampus and osteopenia of the lumbar vertebra and long bones in mice, and causes stress. Various types of stress are associated with increased incidence of cardiovascular disease, but the relationship between occlusal disharmony and cardiovascular disease remain poorly understood. Therefore, in this work, we examined the effects of occlusal disharmony on cardiac homeostasis in bite-opening (BO) mice, in which a 0.7 mm space was introduced by cementing a suitable applicance onto the mandibular incisior. We first examined the effects of BO on the level of serum corticosterone, a key biomarker for stress, and on heart rate variability at 14 days after BO treatment, compared with baseline. BO treatment increased serum corticosterone levels by approximately 3.6-fold and the low frequency/high frequency ratio, an index of sympathetic nervous activity, was significantly increased by approximately 4-fold by the BO treatment. We then examined the effects of BO treatment on cardiac homeostasis in mice treated or not treated with the non-selective β-blocker propranolol for 2 weeks. Cardiac function was significantly decreased in the BO group compared to the control group, but propranolol ameliorated the dysfunction. Cardiac fibrosis, myocyte apoptosis and myocyte oxidative DNA damage were significantly increased in the BO group, but propranolol blocked these changes. The BO-induced cardiac dysfunction was associated with increased phospholamban phosphorylation at threonine-17 and serine-16, as well as inhibition of Akt/mTOR signaling and autophagic flux. These data suggest that occlusal disharmony might affect cardiac homeostasis via alteration of the autonomic nervous system.

In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on masseter and cardiac muscles in mice. In cardiac muscle, chronic β1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In masseter muscle, however, chronic β1-AR stimulation did not induce muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic β2-AR stimulation in masseter muscle induced muscle hypertrophy without histological abnormalities, as in the case of cardiac muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the β1-AR pathway is deleterious and the β2-AR is protective in masseter muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal muscle wasting and weakness.

Although multiple factors influence food bite size, the relationship between food bite size per mouthful and mandible or tongue size remains poorly understood. Here, we examined the correlations between food bite size and the lower dental arch size (an indicator of tongue size) in human subjects with good oral and general health, using fish sausage and bread as test foods. Notably, bite size of both foods was significantly positively correlated with the lower dental arch size, whereas masticatory performance (measured in terms of glucose extraction from a gummy jelly) showed no dependence on bite size. Further, bite size was significantly positively correlated with the body mass index. Our findings suggest that larger bite size is associated with larger tongue size, which might be a contributory factor to obesity.

Chronic administration of clenbuterol (CB), a lipophilic β2-adrenoceptor (β2-AR) agonist, induces skeletal muscle hypertrophy and slow-to-fast fiber–type transitions in mammalian species, but the mechanism and pathophysiological roles of these changes have not been explored. Here, we examined the effects of CB not only on masseter muscle mass, fiber diameter, and myosin heavy chain (MHC) composition, but also on daily muscle activity, a factor influencing muscle phenotype, by means of electromyogram analysis in rats. MHC transition towards faster isoforms was induced by 2-week CB treatment. In addition, daily duty time was increased at 1 day, 1 week, and 2 weeks after the start of CB treatment and its increase was greater at high activity level (6-fold) than at low activity level (2-fold). In order to examine whether these effects of CB were mediated through muscle or CNS β2-AR stimulation, we compared these effects of CB with those of salbutamol (SB), a hydrophilic β2-AR agonist. SB treatment induced masseter hypertrophy and MHC transition, like CB, but did not increase daily activity. These results suggest that CB-mediated slow-to-fast MHC transition with hypertrophy was induced through direct muscle β2-AR stimulation, but the increase of daily duty time was mediated through the CNS. [Supplementary Figures: available only at http://dx.doi.org/10.1254/jphs.12271FP] Keywords:: β2-adrenergic signaling, masseter muscle, electromyogram, myosin heavy chain, hypertrophy

Stimulation of β-adrenergic receptors in cardiac myocytes activates cyclic AMP– dependent protein kinase A (PKA). PKA-mediated phosphorylation of myofibrils decreases their longitudinal stiffness, but its effect on transverse stiffness is not fully understood. We thus examined the effects of PKA treatment on the transverse stiffness of cardiac myofibrils by atomic force microscopy and determined the phosphorylation levels of myofibril components by SDS-PAGE. Transverse stiffness was significantly decreased by PKA treatment concomitantly with increased phosphorylation of troponin I, myosin-binding protein C, and titin (also called connectin). Subsequent treatment with protein phosphatase 1 abrogated these PKA-mediated effects. [Supplementary methods: available only at http://dx.doi.org/10.1254/jphs.13110SC] Keywords:: stiffness, catecholamine, contractility

© 2016 Elsevier LtdBackground Independence from fossil fuels, energy diversification, decarbonisation and energy efficiency are key prerequisites to make a national, regional or continental economy competitive in the global marketplace. As Europe is about to generate 20% of its energy demand from Renewable Energy Sources (RES) by 2020, adequate RES integration and renewable energy storage throughout the entire food cold chain must properly be addressed. Scope and approach Refrigerated warehouses for chilled and frozen foods are large energy consumers and account for a significant portion of the global energy demand. Nevertheless, the opportunity for RES integration in the energy supply of large food storage facilities is often neglected. In situ power generation using RES permits capture of a large portion of virtually free energy, thereby reducing dramatically the running costs and carbon footprint, while enhancing the economic competitiveness. In that context, there exist promising engineering solutions to exploit various renewables in the food preservation sector, in combination with the emerging sustainability-enhancing technology of Cryogenic Energy Storage (CES). Key findings and conclusions Substantial research endeavours are driven by the noble objective to turn the Europe's Energy Union into the world's number one in renewable energies. Integrating RES, in synchrony with CES development and proper control, is capable of both strengthening the food refrigeration sector and improving dramatically the power grid balance and energy system sustainability. Hence, this article aims to familiarise stakeholders of the European and global food preservation industry with state-of-the-art knowledge, know-how, opportunities and professional achievements in the concerned field.

Obesity is well known to be associated with a wide variety of illnesses, and is an increasing problem not only in developed countries but also in developing countries. It is well known that large bite size contributes to excess energy intake and obesity, whereas an increased number of chews before swallowing the food bolus is associated with suppression of obesity. However, the effect of food diameter on bite size per mouthful and on chewing behavior remains poorly understood. Here, we examined the effects of food diameter on bite size and chewing behavior using a masticatory counter during the mastication of stick-type biscuits having the same length (10 cm) and ingredients, but with four different diameters (3.0, 3.5, 4.0, and 8.0 mm). Bite length and bite weight per mouthful were similar among the 3.0, 3.5, and 4.0 mm groups. However, bite length in the 8.0 mm group was significantly smaller, whereas bite weight was significantly greater than in the 3.0/3.5 mm groups. Further, the number of chews gradually increased, whereas the number of chews per bite weight gradually decreased, with an increase of biscuit diameter. These results indicate that a smaller biscuit diameter is associated with a smaller bite weight per mouthful and a greater number of chews per bite weight. This is the first report to quantity the effect of food diameter on bite weight per mouthful and on chewing behavior; these results should be helpful in the design of effective, safe, and low-cost behavioral modification therapy to combat obesity.

When considering camouflage orthodontic treatment of a malocclusion associated with significant facial asymmetry, it is important to define the location of the dental midline. The patient, a 19-year-old Japanese woman, had an anterior open bite and a dental midline discrepancy associated with facial asymmetry. A nonsurgical treatment plan was considered. The main treatment objective was to correct the anterior open bite and the dental midlines in both arches. The dental midline discrepancy was eliminated, and proper overjet and overbite were achieved. Although the facial asymmetry remained, oral esthetics dramatically improved and a favorable occlusion was obtained. The results suggest that appropriately defining the location of the dental midline is critical for successful camouflage treatment of facial asymmetry.

To gain more insight into the molecular mechanism of muscle growth and fiber-type transformations, we analyzed the effects of beta(2)-adrenergic agonist clenbuterol (CB) and/or cyclosporin A (CsA), a potent inhibitor of calcineurin (CaN), on the muscle mass as well as on the mRNA levels of myosin heavy chains (MHC I, IIa, IId/x, IIb), using a real-time RT-PCR with specific primers in rat masseter. In comparison with control, the CB treatment significantly decreased the MHC I mRNA level (p < 0.01), but increased the MHC IId/x mRNA level (p < 0.01), and the CsA treatment significantly decreased the MHC I mRNA level (p < 0.05) in association with the significant decrease in MHC IIb mRNA level (p < 0.05). The CB+CsA treatment significantly decreased the levels of MHC I (p < 0.01) and IIa mRNAs (p < 0.05), but increased the MHC IId/x mRNA level (p < 0.001) in association with a significant decrease in MHC IIb mRNA level (p < 0.01), in comparison with control. The masseter muscle mass was significantly (p < 0.001) increased by either the CB or the CB + CsA treatment, but decreased with the CsA treatment (p < 0.01). These results suggest that in rat masseter muscle, CB has an anabolic action accompanying MHC mRNA I IIa IId/x sequence transition independently of CaN-signaling pathways, and CaN is involved in the type I fiber gene expression and the muscle mass maintenance of type IIb fiber.

To gain more insight into the mechanism of muscle plasticity in response to mechanical overload, we analyzed the effects of bite -opening (BO, 3 mm increase in the vertical dimension for 2 weeks) and/or a calcineurin (CaN) inhibitor, cyclosporin A (CsA, 10 mg/kg body weight, once daily for 2 weeks, ip) treatment on the myosin heavy chain (MHC I, IIa, IId/x, IIb) mRNA levels, using real-time RT-PCR with specific primers and on the muscle mass in rat masseter. As compared with normal control (n = 6), the BO treatment (n = 6) significantly increased the MHC I (p < 0.05) and the IIa mRNA levels (p < 0.01), and the CsA treatment (n = 6) significantly decreased the MHC I mRNA level (p < 0.01) in association with the significant decrease in the MHC IIb mRNA level (p < 0.05). The BO + CsA treatment (n = 6) significantly increased the MHC IIa mRNA level (p < 0.01) in association with the significant decrease in the MHC IIb mRNA level (p < 0.01), as compared with control. The masseter muscle mass was significantly decreased by either the CsA (p < 0.05) or the BO + CsA treatment (p < 0.001), but slightly increased by the BO treatment. These results suggest that in rat masseter the BO treatment produces not only the up-regulation of MHC IIa mRNA independently of CaN-signaling pathways, but also the MHC mRNA transition from IIa to I and the muscle mass maintenance mainly of type IIb fiber through the CaN-signaling pathways.

Background Glucocorticoid has a direct catabolic effect on skeletal muscle, leading to muscle atrophy, but no effective pharmacotherapy is available. We reported that clenbuterol (CB) induced masseter muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct muscle β2-adrenergic receptor stimulation. Thus, we hypothesized that CB would antagonize glucocorticoid (dexamethasone; DEX)-induced muscle atrophy and fast-to-slow MHC isoform transition. Methodology We examined the effect of CB on DEX-induced masseter muscle atrophy by measuring masseter muscle weight, fiber diameter, cross-sectional area, and myosin heavy chain (MHC) composition. To elucidate the mechanisms involved, we used immunoblotting to study the effects of CB on muscle hypertrophic signaling (insulin growth factor 1 (IGF1) expression, Akt/mammalian target of rapamycin (mTOR) pathway, and calcineurin pathway) and atrophic signaling (Akt/Forkhead box-O (FOXO) pathway and myostatin expression) in masseter muscle of rats treated with DEX and/or CB. Results and Conclusion Masseter muscle weight in the DEX-treated group was significantly lower than that in the Control group, as expected, but co-treatment with CB suppressed the DEX-induced masseter muscle atrophy, concomitantly with inhibition of fast-to-slow MHC isoforms transition. Activation of the Akt/mTOR pathway in masseter muscle of the DEX-treated group was significantly inhibited compared to that of the Control group, and CB suppressed this inhibition. DEX also suppressed expression of IGF1 (positive regulator of muscle growth), and CB attenuated this inhibition. Myostatin protein expression was unchanged. CB had no effect on activation of the Akt/FOXO pathway. These results indicate that CB antagonizes DEX-induced muscle atrophy and fast-to-slow MHC isoform transition via modulation of Akt/mTOR activity and IGF1 expression. CB might be a useful pharmacological agent for treatment of glucocorticoid-induced muscle atrophy.

Clenbuterol (CB), a selective β 2‐adrenergic receptor (AR) agonist, induces muscle hypertrophy and counteracts muscle atrophy. However, it is paradoxically less effective in slow‐twitch muscle than in fast‐twitch muscle, though slow‐twitch muscle has a greater density of β‐AR. We recently demonstrated that Epac1 (exchange protein activated by cyclic AMP [cAMP]1) plays a pivotal role in β 2‐AR‐mediated masseter muscle hypertrophy through activation of the Akt and calmodulin kinase II (CaMKII)/histone deacetylase 4 (HDAC4) signaling pathways. Here, we investigated the role of Epac1 in the differential hypertrophic effect of CB using tibialis anterior muscle (TA; typical fast‐twitch muscle) and soleus muscle (SOL; typical slow‐twitch muscle) of wild‐type (WT) and Epac1‐null mice (Epac1KO). The TA mass to tibial length (TL) ratio was similar in WT and Epac1KO at baseline and was significantly increased after CB infusion in WT, but not in Epac1KO. The SOL mass to TL ratio was also similar in WT and Epac1KO at baseline, but CB‐induced hypertrophy was suppressed in both mice. In order to understand the mechanism involved, we measured the protein expression levels of β‐AR signaling‐related molecules, and found that phosphodiesterase 4 (PDE4) expression was 12‐fold greater in SOL than in TA. These results are consistent with the idea that increased PDE4‐mediated cAMP hydrolysis occurs in SOL compared to TA, resulting in a reduced cAMP concentration that is insufficient to activate Epac1 and its downstream Akt and CaMKII/HDAC4 hypertrophic signaling pathways in SOL of WT. This scenario can account for the differential effects of CB on fast‐ and slow‐twitch muscles.