***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Gut-derived hormones , such as GLP-1 , have been proposed to relay information to the brain to regulate appetite . GLP-1 receptor agonists , currently used for the treatment of type 2 diabetes ( T2DM ) , improve glycemic control and stimulate satiety , leading to decreases in food intake and body weight . We hypothesized that food intake reduction after GLP-1 receptor activation is mediated through appetite- and reward-related brain areas . Obese T2DM patients and normoglycemic obese and lean individuals ( n = 48 ) were studied in a r and omized , crossover , placebo-controlled trial . Using functional MRI , we determined the acute effects of intravenous administration of the GLP-1 receptor agonist exenatide , with or without prior GLP-1 receptor blockade using exendin 9 - 39 , on brain responses to food pictures during a somatostatin pancreatic-pituitary clamp . Obese T2DM patients and normoglycemic obese versus lean subjects showed increased brain responses to food pictures in appetite- and reward-related brain regions ( insula and amygdala ) . Exenatide versus placebo decreased food intake and food-related brain responses in T2DM patients and obese subjects ( in insula , amygdala , putamen , and orbitofrontal cortex ) . These effects were largely blocked by prior GLP-1 receptor blockade using exendin 9 - 39 . Our findings provide novel insights into the mechanisms by which GLP-1 regulates food intake and how GLP-1 receptor agonists cause weight loss Objectives Previous fMRI studies have demonstrated that glucose decreases the hypothalamic BOLD response in humans . However , the mechanisms underlying the CNS response to glucose have not been defined . We recently demonstrated that the slowing of gastric emptying by glucose is dependent on activation of the gut peptide cholecystokinin ( CCK1 ) receptor . Using physiological functional magnetic resonance imaging this study aim ed to determine the whole brain response to glucose , and whether CCK plays a central role . Experimental design Changes in blood oxygenation level-dependent ( BOLD ) signal were monitored using fMRI in 12 healthy subjects following intragastric infusion ( 250 ml ) of : 1 M glucose + predosing with dexloxiglumide ( CCK1 receptor antagonist ) , 1 M glucose + placebo , or 0.9 % saline ( control ) + placebo , in a single-blind , r and omised fashion . Gallbladder volume , blood glucose , insulin , and GLP-1 and CCK concentrations were determined . Hunger , fullness and nausea scores were also recorded . Principal observations Intragastric glucose elevated plasma glucose , insulin , and GLP-1 , and reduced gall bladder volume ( an in vivo assay for CCK secretion ) . Glucose decreased BOLD signal , relative to saline , in the brainstem and hypothalamus as well as the cerebellum , right occipital cortex , putamen and thalamus . The timing of the BOLD signal decrease was negatively correlated with the rise in blood glucose and insulin levels . The glucose + dex arm highlighted a CCK1-receptor dependent increase in BOLD signal only in the motor cortex . Conclusions Glucose induces site-specific differences in BOLD response in the human brain ; the brainstem and hypothalamus show a CCK1 receptor-independent reduction which is likely to be mediated by a circulatory effect of glucose and insulin , whereas the motor cortex shows an early dexloxiglumide-reversible increase in signal , suggesting a CCK1 receptor-dependent neural pathway Abstract Background : Although protein-rich plant foods have recently been touted as an equivalent to animal products , limited data exist regarding the effects of animal vs. plant proteins on appetite , satiety , and subsequent food intake . Objective : The objective was to determine whether a high-protein beef lunch alters the appetitive , hormonal , and neural signals controlling food intake regulation vs. a macronutrient and fiber – matched ( MF ) or serving size – matched ( SS ) soy lunch in healthy adults . Methods : A r and omized , double-blind , crossover design study was completed in 21 adults ( aged 23 ± 1 y ; body mass index : 23.8 ± 0.6 kg/m2 ; mean ± SEM ) to compare 400-kcal MF and SS lunches varying in protein quality . The MF lunches contained 24-g beef protein or 24-g soy protein , whereas the SS lunches contained 1 serving of beef ( 24-g protein/1-g fiber ) or soy ( 14-g protein/5-g fiber ) . Pre- and postlunch appetite question naires and blood sampling were completed over an 8-h period until dinner was voluntarily requested . In addition , pre- and postlunch functional MRI brain scans were completed to assess neural activation in response to food stimuli . Results : On average , dinner was requested at ∼250 ± 20 min postlunch with no differences between beef vs. soy within the MF and SS conditions . Furthermore , no differences in hunger , fullness , peptide YY , or glucagon-like peptide-1 responses were observed after the beef vs. soy lunches within the MF and SS conditions . The SS beef meal led to reductions in anterior cingulate activation ( −22 ± 6 % ) vs. soy ( + 7 ± 9%;P < 0.01 ) and greater reductions in insular activation ( −30 ± 6 % ) vs. SS soy ( −7 ± 10%;P < 0.01 ) . The participants consumed ∼945 ± 78 kcal after the MF meals and 910 ± 74 kcal after the SS meals with no differences between beef vs. soy . Conclusions : When comparing 2 high- quality protein sources , such as beef and soy , the type of protein consumed within a mixed meal elicited very little effect on appetite , satiety , and food intake in healthy adults . This study was registered at clinical trials.gov as NCT02285907 Drug addiction is a chronic , relapsing brain disorder . The identification of biomarkers that render individuals vulnerable for the transition from occasional drug use to addiction is of key importance to develop early intervention strategies . The aim of the present study was to prospect ively assess brain structural markers for escalating drug use in two independent sample s of occasional amphetamine-type stimulant users . At baseline occasional users of amphetamine and 3,4-methylenedioxymethamphetamine ( cumulative lifetime use ≤10 units ) underwent structural brain imaging and were followed up at 12 months and 24 months ( Study 1 , n = 38 ; Study 2 , n = 28 ) . Structural vulnerability markers for escalating amphetamine-type drug use were examined by comparing baseline grey matter volumes of participants who increased use with those who maintained or reduced use during the follow-up period . Participants in both sample s who subsequently increased amphetamine-type drugs use displayed smaller medial prefrontal cortex volumes and , additionally , in the basolateral amygdala ( Study 1 ) and dorsal striatum ( Study 2 ) . In both sample s the baseline volumes were significantly negatively correlated with stimulant use during the subsequent 12 and 24 months . Additional multiple regression analyses on the pooled data sets revealed some evidence of a compound-specific association between the baseline volume of the left basolateral amygdala and the subsequent use of amphetamine . These findings indicate that smaller brain volumes in fronto-striato-limbic regions implicated in impulsivity and decision-making might render an individual vulnerable for the transition from occasional to escalating amphetamine-type stimulant use Insulin and cortisol play a key role in the regulation of energy homeostasis , appetite , and satiety . Little is known about the action and interaction of both hormones in brain structures controlling food intake and the processing of neurovisceral signals from the gastrointestinal tract . In this study , we assessed the impact of single and combined application of insulin and cortisol on resting regional cerebral blood flow ( rCBF ) in the insular cortex . After st and ardized periods of food restriction , 48 male volunteers were r and omly assigned to receive either 40 IU intranasal insulin , 30 mg oral cortisol , both , or neither ( placebo ) . Continuous arterial spin labeling ( CASL ) sequences were acquired before and after pharmacological treatment . We observed a bilateral , locally distinct rCBF increase after insulin administration in the insular cortex and the putamen . Insulin effects on rCBF were present regardless of whether participants had received cortisol or not . Our results indicate that insulin , but not cortisol , affects blood flow in human brain structures involved in the regulation of eating behavior BACKGROUND Ghrelin , which is a stomach-derived hormone , increases with fasting and energy restriction and may influence eating behaviors through brain hedonic reward-cognitive systems . Therefore , changes in plasma ghrelin might mediate counter-regulatory responses to a negative energy balance through changes in food hedonics . OBJECTIVE We investigated whether ghrelin administration ( exogenous hyperghrelinemia ) mimics effects of fasting ( endogenous hyperghrelinemia ) on the hedonic response and activation of brain-reward systems to food . DESIGN In a crossover design , 22 healthy , nonobese adults ( 17 men ) underwent a functional magnetic resonance imaging ( fMRI ) food-picture evaluation task after a 16-h overnight fast ( Fasted-Saline ) or after eating breakfast 95 min before scanning ( 730 kcal , 14 % protein , 31 % fat , and 55 % carbohydrate ) and receiving a saline ( Fed-Saline ) or acyl ghrelin ( Fed-Ghrelin ) subcutaneous injection before scanning . One male subject was excluded from the fMRI analysis because of excess head motion , which left 21 subjects with brain-activation data . RESULTS Compared with the Fed-Saline visit , both ghrelin administration to fed subjects ( Fed-Ghrelin ) and fasting ( Fasted-Saline ) significantly increased the appeal of high-energy foods and associated orbitofrontal cortex activation . Both fasting and ghrelin administration also increased hippocampus activation to high-energy- and low-energy-food pictures . These similar effects of endogenous and exogenous hyperghrelinemia were not explicable by consistent changes in glucose , insulin , peptide YY , and glucagon-like peptide-1 . Neither ghrelin administration nor fasting had any significant effect on nucleus accumbens , cau date , anterior insula , or amygdala activation during the food-evaluation task or on auditory , motor , or visual cortex activation during a control task . CONCLUSIONS Ghrelin administration and fasting have similar acute stimulatory effects on hedonic responses and the activation of corticolimbic reward-cognitive systems during food evaluations . Similar effects of recurrent or chronic hyperghrelinemia on an anticipatory food reward may contribute to the negative impact of skipping breakfast on dietary habits and body weight and the long-term failure of energy restriction for weight loss BACKGROUND & AIMS In human beings , as in most vertebrates , the release of the intestinal peptide cholecystokinin ( CCK ) by ingested food plays a major role both in digestion and the regulation of further food intake , but the changes in brain function and their underlying activation mechanisms remain unknown . Our aim was to explore , using a novel physiologic magnetic resonance imaging approach , the temporospatial brain activation matrix , in response to ingestion of a lipid meal and , by use of a CCK-1 receptor antagonist , to define the role of CCK in this activation . METHODS We studied , in 19 healthy subjects , the brain activation responses to ingested lipid ( dodecanoic acid ) or saline ( control ) with magnetic resonance imaging .  Gallbladder volume , plasma CCK levels , and subjective hunger and fullness scores were also recorded . The experiment was then repeated , with and without prior administration of the CCK-1 receptor antagonist dexloxiglumide ( 600 mg orally ) with a controlled , r and omized order , latin-square design . RESULTS Ingested lipid activated bilaterally a matrix of brain areas , particularly the brain stem , pons , hypothalamus , and also cerebellum and motor cortical areas . These activations were abolished by dexloxiglumide , indicating a CCK-mediated pathway , independent of any nutrient-associated awareness cues . CONCLUSION The identification of these activations now defines the lipid-activated brain matrix and provides a means by which the gut-derived homeostatic mechanisms of food regulation can be distinguished from secondary sensory and hedonic cues , thereby providing a new approach to exploring aberrant human gastrointestinal responses and eating behavior BACKGROUND Qualitative aspects of diet influence eating behavior , but the physiologic mechanisms for these calorie-independent effects remain speculative . OBJECTIVE We examined effects of the glycemic index ( GI ) on brain activity in the late postpr and ial period after a typical intermeal interval . DESIGN With the use of a r and omized , blinded , crossover design , 12 overweight or obese men aged 18 - 35 y consumed high- and low-GI meals controlled for calories , macronutrients , and palatability on 2 occasions . The primary outcome was cerebral blood flow as a measure of resting brain activity , which was assessed by using arterial spin-labeling functional magnetic resonance imaging 4 h after 
    Output:
    
Of the 349 studies published before July 2016 identified in the data base search , 40 were included ( 27 on healthy and 13 on obese subjects).Plasma  level of ghrelin positively correlate with activation in the pre‐frontal cortex , amygdala and insula and negatively subcortical areas .In contrast , the plasma levels of glucose , insulin , leptin , PYY , GLP‐1 affect the same brain in the opposite direction .
Our systematic review suggests that the plasma level of ghrelin , the gut hormone promoting appetite , is positively correlated with activation in the pre‐frontal cortex ( PFC ) , amygdala and insula and negatively correlated with activation in subcortical areas such as the hypothalamus .
In contrast , the plasma levels of glucose , insulin , leptin , PYY , GLP‐1 affect the same brain regions conversely .