U kiss soohyun and jo kwon gain dating

U-Kiss World News | ann-estetyka.info | Page 14

u kiss soohyun and jo kwon gain dating

Do you know your kpop trivia, well take this quiz find out! Which idol was rumored to be dating JoKwon? A. Gain. B. Soohyun. C. Taehyun. D. It would be upward scant that you are inactive. you can now find the deep dating · isde practica juridica online dating · u kiss soohyun and jo kwon gain dating. If you find you're not compatible with your bias, you can always check Jokwon ( 2AM/Solo Singer) – Aug 28, AJ (U Kiss) – June 4, though; The Dog was born with his defenses up, you will have to gain their.

After he played a gay character on that show, his surprise at having his sexuality questioned in real life seemed like genuine straight confusion from someone never having to deal with that sorta thing. I see Sunggyu and Sungyeol are definitely the straightest members in Infinite. The guy is sex! I think he's straight but I honestly don't know what to make of his butt-grabbing hobby.

u kiss soohyun and jo kwon gain dating

He likes male butts? Even I suspected him to be dating Key I still think they're dating or at least interested in each other. The Taiwan incident, the way both Woohyun and Key acted after that and his questionable ideal type: I honestly think Woohyun escaped all the hate just by doing nonstop aegyo and throwing hearts which seem fake and mechanical to me tbh LMAO Myungsoo: I had massive amounts of delusional evidence that he's gay. He's weirder than most people think tbvh.

An awkward and weird guy with no self esteem. He even gives an eccentric feeling when you meet him irl. He seems very clingy and obsessive type and doesn't let go easily. Woohyun once mentioned that L is very naive despite his appearance. I have seen him forcefully hug his members even if they don't want to hug him in public. Even with all this clinging, no one thought he's gay?

u kiss soohyun and jo kwon gain dating

I doubt everyone knows he's gay and yet the ultra homophobic Koreans are okay with him while they hate Sungjong who is not even half as clingy as Myungsoo. I wonder why Woolim never tried to 'straighten' him like Sungjong. Any inkling of imperfection and he's ripped apart.

He's never anything enough. I don't understand why Myungsoo in particular seems to garner so much unwarranted criticism though. He sings better than Sungyeol who barely has one line in every song; while Sungyeol is pitied for not having much lines, Myungsoo gets all the hate for his bad singing.

The CEO tore his shirt when he was obsessed with plaid shirts and wore different colours of them. Yet no one did anything about Hoya who is obsessed with purple and practically has everything in purple colour The gays LOVE him and he was voted the most popular boy amongst the Korean gays.

Earlier this year, several men shouted his name when he made an appearance in public. Certain addictive behaviors, such as failed attempts to reduce food intake or continued feeding in spite of negative fallout, manifest in troubled eating patterns [ 27 ].

The brain also appears to respond to highly palatable foods in some similar fashions as it does to addictive drugs [ 28 ]. The current hypothesis is that certain foods or ingredients added to foods might trigger the addictive process in susceptible people [ 29 ]. The addictive process is more or less viewed as a chronic relapsing issue dependent upon factors that elevate cravings for food or food-related substances and heighten the state of pleasure, emotion, and motivation [ 3031323334 ].

The Yale Rudd Center for Food Policy and Obesity, a non-profit research and public policy organization, reported in striking similarities in the use and withdrawal patterns of sugar and classic drugs of abuse, as well as reciprocal correlations between food intake and substance abuse e.

This raises the possibility that palatable foods and classic addictive substances may compete for similar neurophysiological pathways [ 3536 ].

The Rudd Center helped create the Yale Food Addiction Scale YFASwhich is designed to identify signs of addiction exhibited towards certain types of food with high fat and sugar contents [ 3738 ]. Gearhardt and her colleague [ 39 ] have recently examined brain activation to food cues in patients with various scores on the food addiction scale.

The patients were either signaled for impending delivery of a chocolate milkshake or a tasteless control solution, or were given a chocolate milkshake or a tasteless solution [ 39 ]. The results showed an association between higher food addiction scores and increased activation of brain regions encoding motivation in response to food cues, such as the amygdala AMYanterior cingulate cortex ACCand orbitofrontal cortex OFC.

It was concluded that addictive individuals are more likely to react to substance cues, and that the anticipation of a reward when a cue is noticed could contribute to compulsive eating [ 39 ]. In general, food addiction is not well defined and may be associated with substance use disorders [ 40 ] and eating disorders. It is noteworthy that the DSM-5 has proposed revisions recognizing binge eating disorder [ 41 ] as a free-standing diagnosis and renaming the category of Eating Disorders as Eating and Feeding Disorders.

PWS patients display many addictive eating behaviors [ 43 ]. Neuroimaging studies in this naturally occurring human eating disorder model may uncover neurophysiological mechanisms governing food addiction or loss of control of eating in general. One characteristic of the disease is a marked obsessive drive to overeat not only food but also neutral non-food objects.

Excessive and pathologic reinforcement produced by the ingested items themselves might contribute to this phenomenon [ 424344454647484950 ]. Functional neuroimaging studies have investigated the abnormalities of eating-related neural circuitry using visual cues in PWS patients [ 44 ]. In response to visual high- versus low-calorie food stimulation after glucose administration, the PWS patients exhibited a delayed signal reduction in the hypothalamus HPALinsula, ventromedial prefrontal cortex VMPFCand nucleus accumbens NAc [ 44 ], but hyperactivity in limbic and paralimbic regions such as the AMY that drive eating behavior and in regions such as the medial prefrontal cortex MPFC that suppress food intake [ 4751 ].

Our group performed a resting-state fMRI RS-fMRI study combined with functional connectivity FC analysis and identified the alterations of FC strength among the brain regions in the default mode network, core network, motor sensory network, and prefrontal cortex network, respectively [ 53 ].

We recently utilized RS-fMRI and Granger causality analysis techniques to investigate the interactive causal influences among key neural pathways underlying overeating in PWS. In summary, PWS is the extreme end of human cases of obesity and uncontrollable eating behaviors. Investigation of the neurophysiological underpinning of PWS and its association with substance dependence may aid better understanding of appetite control and food addiction [ 3943 ].

Hormones and Gut Peptides Many peripheral hormones participate in central nervous system CNS control of appetite and food intake, food reward, or addiction. Both palatable foods and drugs are able to activate the mesolimbic dopamine DA reward system essential for addiction regulation in humans and animals [ 435455565758 ]. Hunger and satiety signals from adipose tissue leptinthe pancreas insulinand the gastrointestinal tract cholecystokinin CCKglucagon-like peptide-l GLP-1peptide YY PYYand ghrelin are involved in relaying information about energy status through the neural hormonal gut-brain axis primarily targeting the hypothalamus HPAL and brainstem [ 58 ], and may directly or indirectly interact with the midbrain DA pathways to impact feeding [ 596061 ].

Leptin An anorexigenic hormone synthesized from adipose tissue, leptin regulates lipid metabolism by stimulating lipolysis and inhibiting lipogenesis [ 62 ]. Leptin crosses the blood-brain barrier via a saturable transport system and communicates the periphery metabolic status energy storage to the hypothalamic regulatory centers [ 63 ].

Once bound to its central receptor, leptin down-regulates appetite-stimulating neuropeptides e. Genetic defects in leptin and leptin receptors result in severe early onset obesity in children [ 64 ]. Leptin concentration in the blood is elevated in obesity, promoting a leptin resistance that renders the elevated leptin futile in curbing appetite and obesity. The presence of leptin resistance may offer a partial explanation for severe hyperphagia in PWS patients whose serum leptin levels are quite high [ 64 ].

People in the process of becoming addicted to food may also have leptin resistance, which could lead to overeating [ 65 ]. As one fMRI study demonstrated, supplemented leptin diminished food reward and enhanced satiety during food consumption by modulating neuronal activity in the striatum in leptin-deficient human subjects [ 66 ].

Leptin monotherapy, however, has not been successful in reducing food intake and weight gain in obese humans as originally hoped, possibly due to preexisting leptin resistance in obesity [ 67 ].

On the other hand, a low-dose leptin supplement may be useful for tempering the reward value of food [ 68 ] and helping to maintain lost weight. Insulin Insulin is a pancreatic hormone critical for maintenance of glucose homeostasis. Insulin levels rise after a meal to keep blood glucose in check. The excess glucose is converted and stored in the liver and muscle as glycogen, and as fat in adipose tissues. Insulin concentrations vary with adiposity, and the amount of visceral fat is negatively correlated with insulin sensitivity [ 69 ].

Fasting and postprandial insulin are higher in obese than in lean individuals [ 70 ]. Insulin can penetrate the blood-brain barrier and binds to receptors in the arcuate nucleus of the hypothalamus to decrease food intake [ 71 ]. Central insulin resistance may occur in obesity, similarly to the central leptin resistance that is thought to be consequential to high fat consumption or obesity development [ 7273 ].

A positron emission tomography PET study identified insulin resistance in the striatum and insula areas of the brain and suggested that such a resistance may require higher brain insulin levels in order to adequately experience the reward and the interoceptive sensations of eating [ 74 ].

WATCH: Meet Justin Bieber’s Gayer Korean Equivalent, Jo Kwon / Queerty

Like leptin, insulin is capable of modulating the DA pathway and associated eating behaviors. Leptin and insulin resistance in the brain DA pathways may result in heightened intake of palatable foods as compared to leptin- and insulin-sensitive conditions in order to generate a sufficient reward response [ 75 ]. The interplay between the central and peripheral hormonal signaling pathways is complex.

For example, ghrelin stimulates dopaminergic reward pathways, while leptin and insulin inhibit these circuits. Moreover, signaling circuits in both the HPLA and the ARC receive afferent peripheral sensory signals and project and relay the information to other regions of the brain, including the midbrain dopaminergic reward center [ 31 ].

Ghrelin Mainly secreted by the stomach, ghrelin is an orexigenic peptide that acts on hypothalamic neurons containing ghrelin receptors to exert central metabolic effects [ 76 ].

U-KISS (ユーキス) – A Shared Dream (CC Lyrics)

Ghrelin increases food intake in humans by both peripheral and central mechanisms involving interplay between the stomach, the HPAL, and the hypophysis [ 7778 ]. Ghrelin appears to be an initiator of feeding with peak serum levels prior to food ingestion and reduced levels thereafter [ 79 ].

Ghrelin may chronically impact energy equilibrium, considering that prolonged ghrelin administration enlarges adiposity [ 7780 ]. Serum ghrelin levels are lower in the obese relative to normal weight individuals and characteristically increase with obesity reduction, demonstrating a negative correlation with high BMIs [ 8182 ]. Ghrelin activates the brain regions important for hedonic and incentive responses to food cues [ 83 ].

This includes activation of dopamine neurons in the VTA and increased dopamine turnover in the NAc of the ventral striatum [ 84 ]. Following food ingestion, PYY is released from the L-cells in the distal segment of the small gut. It reduces the rate of intestinal motility and gallbladder and gastric emptying and therefore decreases appetite and augments satiety [ 8586 ].

Obese people secrete less PYY than non-obese people and have relatively lower levels of serum ghrelin [ 88 ]. Thus, PYY replacement may be used to treat overweight and obesity [ 8889 ]. The extent of reduction was quite impressive in the former case.

Although obese persons are shown to have lower circulating levels of PYY postprandially, they also seem to display normal sensitivity to the anorectic effect of PYY Taken together, obesity may bias the PYY sensitivity issue, and the anorectic effect of PYY could serve as a therapeutic mechanism for developing anti-obesity drugs [ 90 ].

Peripheral administration of GLP-1 decreases food intake and increases fullness in humans in part by slowing gastric emptying and promoting gastric distension [ 93 ].

Plasma levels of GLP-1 are higher before and after food intake in lean as compared to obese individuals, while the latter are associated with lower fasting GLP-1 and an attenuated postprandial release [ 94 ].

Ukiss kevin and soohyun talks about they gay rumors

Restrictive bariatric procedures are an effective means of reducing obesity. Currently, data are limited regarding changes in GLP-1 concentrations in obese patients after surgeries [ 95 ]. Cholecystokinin CCK Cholecystokinin CCKan endogenous peptide hormone present in the gut and the brain, helps control appetite, ingestive behavior, and gastric emptying via both peripheral and central mechanisms.

CCK also impacts physiological processes related to anxiety, sexual behavior, sleep, memory, and intestinal inflammation [ 95 ]. These various hormones do not appear to differ significantly in physiological functions. It is a potent stimulator of pancreatic digestive enzymes and bile from the gallbladder [ 63 ]. CCK delays gastric emptying and promotes intestinal motility.

As a neuropeptide, CCK activates receptors on vagal afferent neurons, which transmit satiety signals to the dorsomedial hypothalamus.

This action suppresses orexigenic neuropeptide NPY and provides feedback to reduce meal size and meal duration [ 97 ].

WATCH: Meet Justin Bieber’s Gayer Korean Equivalent, Jo Kwon / Queerty

In summary, peripheral hormonal signals released from the GI tract ghrelin, PYY, GLP-1, and CCKpancreas insulinand adipose tissue leptin constitute a key component in the gut-brain axis-mediated control of appetite, energy expenditure, and obesity. While leptin and insulin may be considered more long-term regulators of energy balance, ghrelin, CCK, peptide YY, and GLP-1 are sensors related to meal initiation and termination and hence affect appetite and body weight more acutely.

These hormones and peptides alter appetite and eating behaviors by acting on hypothalamic and brainstem nuclei and perhaps on the dopaminergic pathway in the midbrain reward center; they have demonstrated potential as therapeutic targets for anti-obesity treatments. Neuroimaging Studies Neuroimaging is a common tool to investigate the neurological basis of appetite and body weight regulation in humans in terms of cue-induced brain responses and structural analyses [ 98 ].

u kiss soohyun and jo kwon gain dating

Hyper- or hypo-activation in response to food intake or food cues in multiple brain regions implicated in reward e. Functional Neuroimaging By measuring brain responses to pictures of high-calorie foods e. These results illuminate the relationship between cortical responses to food cues and obesity and provide important insights into the development and maintenance of obesity [ ].

They found that average food consumption during the first 15 days was lower in DBS-treated animals than in non-stimulated animals. DBS increased metabolism in the mammillary body, subiculum hippocampal area, and AMY, while a decrease in metabolism was recorded in the thalamus, caudate, temporal cortex, and cerebellum []. DBS produced significant changes in brain regions associated with the control of food intake and brain reward, presumably by ameliorating the impaired hippocampal functioning seen in obese rats.

The smaller weight gain in the DBS group suggests that this technique could be considered as an option for the treatment of obesity [ ].