TY  - JOUR
AB  - The hypothalamus has an abundant expression of sweet taste receptors that play a role in glucose sensing and energy homeostasis. Evidence suggests that liking "sweets" can be associated with weight gain, but the relationship between sweet taste preference and hypothalamic regulation of appetite is unknown. This study tested the hypothesis that sweet taste preference is associated with increased hypothalamic activation in response to glucose (a purported neural marker for weight gain risk) and greater longitudinal increases in body mass index (BMI). Fifty-four adults aged 18-35 years with a mean (± SD) BMI of 27.99 ± 5.32 kg/m2 completed the study. Height and weight were measured at baseline and 6-12 months later in a subset of 36 participants. Sweet taste preference was assessed via the Monell 2-series, forced-choice tracking procedure. Arterial spin labeling magnetic resonance imaging was performed before and after oral glucose ingestion to determine hypothalamic blood flow response to glucose. Linear models were used to examine relationships between sweet taste preference and the hypothalamic response to glucose and longitudinal changes in BMI, adjusting for age, sex, and baseline BMI. Sweet taste preference was positively associated with glucose-linked hypothalamic blood flow (beta = 0.017, p = 0.043), adjusted for age, sex and BMI. We also observed a positive association between sweet taste preference and longitudinal change in BMI (beta = 0.088, p = 0.015), adjusted for age, sex and baseline BMI. These findings suggest that heightened sweet taste preference is associated with glucose-linked hypothalamic activation and may be linked to increased susceptibility for weight gain.
AU  - Yunker, A.G.*
AU  - Chakravartti, S.P.*
AU  - Kullmann, S.
AU  - Veit, R.
AU  - Angelo, B.*
AU  - Jann, K.*
AU  - Monterosso, J.R.*
AU  - Page, K.A.*
C1  - 68109
C2  - 54587
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
TI  - Sweet taste preference is associated with greater hypothalamic response to glucose and longitudinal weight gain.
JO  - Physiol. Behav.
VL  - 270
PB  - Pergamon-elsevier Science Ltd
PY  - 2023
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - Previous experiments of our group have demonstrated that preprandial processing of food cues attenuates postprandial blood glucose excursions. Here we systematically re-evaluated the glucose-lowering effect of visual food cues by submitting 40 healthy fasted men (20 normal-weight men, mean age 24.8 +/- 3.7 years, BMI 21.9 +/- 0.3 kg/m(2); 20 obese men, 26.8 +/- 4.2 years, 34.3 +/- 1.3 kg/m(2)) to an oral glucose tolerance test (OGTT) following exposure to pictures of high-calorie food items versus neutral items. OGTT-related changes in blood concentrations of glucose and relevant glucoregulatory hormones including GLP-1 were assessed and analyzed according to the oral minimal model. Independent of body weight, food-cue compared to neutral stimulus presentation reduced postprandial concentrations of glucose (p = 0.041), insulin (p = 0.026) and C-peptide (p = 0.007); accordingly, oral minimal model analyses yielded a food-cue induced decrease of dynamic-phase insulin secretion (p = 0.036). We also observed a trend towards lower GLP-1 levels directly after food cue stimulation in both body weight groups (p = 0.057), as well as a trend towards decreased heart rate (p = 0.093) and significantly decreased diastolic blood pressure (p = 0.019). While we did not detect indicators of an early rise in insulin levels in terms of a 'cephalic phase insulin response', our findings support the assumption that preprandial processing of food cues exerts marked effect on postprandial glucose regulation, with possible contributions of changes in GLP-1. The mechanisms linking food cue exposure and glucoregulatory improvements should be investigated in greater detail, to potentially open new treatment options for metabolic dysfunctions.
AU  - Brede, S.*
AU  - Lutzke, B.*
AU  - Albers, E.*
AU  - Dalla-Man, C.*
AU  - Cobelli, C.*
AU  - Hallschmid, M.
AU  - Klement, J.*
AU  - Lehnert, H.*
C1  - 59894
C2  - 49104
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
TI  - Visual food cues decrease blood glucose and glucoregulatory hormones following an oral glucose tolerance test in normal-weight and obese men.
JO  - Physiol. Behav.
VL  - 226
PB  - Pergamon-elsevier Science Ltd
PY  - 2020
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - Background Reward sensitivity can generalize across domains, but evidence for generalization of suppressive reward-related stimulation is sparse, especially in the context of interoceptive nutrient-related stimuli. We hypothesized that subliminal fatty acid-induced gut-brain signals could attenuate sensitivity to exteroceptive rewards, not only within the food domain but also across domains.Method Intragastric infusion of 2.5 g lauric acid (fat condition) or saline (saline condition) was administered to 59 healthy heterosexual male volunteers in a blinded fashion. To assess whether the resulting interoceptive signals attenuate reward sensitivity within the food domain, participants rated the palatability of food images and performed a progressive ratio task. To assess whether such attenuation effect generalizes to the sexual and financial reward domains, participants rated attractiveness of female face images and performed an intertemporal monetary choice task.Results Participants' ratings of food images were lower (F-1,F-172 = 4.51, p = 0.035, Cohen's d: -0.20) in the fat condition. The progressive ratio task terminated earlier in the fat condition compared to saline (F-1,F-52 = 4.17, p = 0.046, odds ratio = 0.31, 95%CI [0.11, 0.98]). Participants' ratings of female face images did not differ between conditions (F-1,F-172= 1.85, p= 0.19, Cohen's d: -0.15). Moreover, the monetary discounting rate did not differ significantly between conditions.Conclusion Overall, these findings suggest a domain-specific effect of subliminal fatty acid infusion on decreasing reward sensitivity.
AU  - Zhao, D.
AU  - Moeini-Jazani, M.*
AU  - Weltens, N.*
AU  - Van Gils, M.*
AU  - Tack, J.*
AU  - Warlop, L.*
AU  - Van Oudenhove, L.*
C1  - 58693
C2  - 48454
CY  - The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
TI  - Subliminal fatty acid-induced gut-brain signals attenuate sensitivity to exteroceptive rewards in food but not in sex or financial domains, in healthy men.
JO  - Physiol. Behav.
VL  - 219
PB  - Pergamon-elsevier Science Ltd
PY  - 2020
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - The risk of weight gain is especially related to disinhibition, which indicates the responsiveness to external food stimuli with associated disruptions in eating control. We adapted a food-related version of the attention network task and used functional magnetic resonance imaging to study the effects of disinhibition on attentional networks in 19 normal-weight participants. High disinhibition scores were associated with a rapid reorienting response to food pictures after invalid cueing and with an enhanced alerting effect of a warning cue signalizing the upcoming appearance of a food picture. Imaging data revealed activation of a right-lateralized ventral attention network during reorienting. The faster the reorienting and the higher the disinhibition score, the less activation of this network was observed. The alerting contrast showed activation in visual, temporo-parietal and anterior sites. These modulations of attentional networks by food-related disinhibition might be related to an attentional bias to energy dense and palatable food and increased intake of food in disinhibited individuals.
AU  - Hege, M.A.
AU  - Stingl, K.T.*
AU  - Veit, R.
AU  - Preissl, H.
C1  - 50636
C2  - 42534
CY  - Oxford
SP  - 84-92
TI  - Modulation of attentional networks by food-related disinhibition.
JO  - Physiol. Behav.
VL  - 176
PB  - Pergamon-elsevier Science Ltd
PY  - 2017
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - CONTEXT: Activity of the hypothalamus - the major brain area controlling peripheral metabolism - is specifically modulated by insulin. Research in animals suggests that brain insulin action influences pancreatic insulin secretion. OBJECTIVE: We investigated the association between hypothalamic insulin sensitivity and pancreatic insulin secretion in humans. DESIGN AND SETTING: This was a clinical-experimental trial in a university hospital setting. PARTICIPANTS: 48 healthy volunteers (21 women and 27 men) were included. MAIN OUTCOME MEASURES: Insulin sensitivity of the hypothalamus was quantified by cerebral blood flow (CBF) using MRI in combination with intranasal insulin administration. On a different day, a 75g oral glucose tolerance test with glucose, insulin, and C-peptide levels measured at five time points was performed. Three established insulin secretion indices (insulinogenic index [IGI], corrected insulin response [CIR], and AUCC-peptide0-30/AUCglucose0-30) were then analyzed for correlations with hypothalamic insulin sensitivity independent of whole-body insulin sensitivity. RESULTS: Hypothalamic insulin sensitivity showed a significant association with all three investigated insulin secretion indices (IGI p=0.0043; CIR p=0.06; AUCCpep0-30/AUCgluc0-30 p=0.0179). Participants with a strong hypothalamic insulin effect (i.e. decreased CBF after intranasal insulin administration) had lower insulin secretion during the OGTT, whereas participants with hypothalamic insulin resistance had substantially higher insulin secretion. No correlations with the occipital cortex, a control region, were detected. CONCLUSIONS: Our data suggest that hypothalamic insulin resistance might contribute to pancreatic insulin hypersecretion. Alternatively, common pathogenetic mechanisms could introduce both brain insulin resistance and beta cell hypersecretion.
AU  - Kullmann, S.
AU  - Fritsche, A.
AU  - Wagner, R.
AU  - Schwab, S.*
AU  - Häring, H.-U.
AU  - Preissl, H.
AU  - Heni, M.
C1  - 50830
C2  - 42900
CY  - Oxford
SP  - 134-138
TI  - Hypothalamic insulin responsiveness is associated with pancreatic insulin secretion in humans.
JO  - Physiol. Behav.
VL  - 176
PB  - Pergamon-elsevier Science Ltd
PY  - 2017
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - In the face of the alarming prevalence of obesity and its associated metabolic impairments, it is of high basic and clinical interest to reach a complete understanding of the central nervous pathways that establish metabolic control. In recent years, the hypothalamic neuropeptide oxytocin, which is primarily known for its involvement in psychosocial processes and reproductive behavior, has received increasing attention as a modulator of metabolic function. Oxytocin administration to the brain of normal-weight animals, but also animals with diet-induced or genetically engineered obesity reduces food intake and body weight, and can also increase energy expenditure. Up to now, only a handful of studies in humans have investigated oxytocin's contribution to the regulation of eating behavior. Relying on the intranasal pathway of oxytocin administration, which is a non-invasive strategy to target central nervous oxytocin receptors, these experiments have yielded some promising first results. In normal-weight and obese individuals, intranasal oxytocin acutely limits meal intake and the consumption of palatable snacks. It is still unclear to which extent - or if at all - such metabolic effects of oxytocin in humans are conveyed or modulated by oxytocin's impact on cognitive processes, in particular on psychosocial function. We shortly summarize the current literature on oxytocin's involvement in food intake and metabolic control, ponder potential links to social and cognitive processes, and address future perspectives as well as limitations of oxytocin administration in experimental and clinical contexts.
AU  - Spetter, M.S.*
AU  - Hallschmid, M.
C1  - 50704
C2  - 42483
CY  - Oxford
SP  - 31-39
TI  - Current findings on the role of oxytocin in the regulation of food intake.
JO  - Physiol. Behav.
VL  - 176
PB  - Pergamon-elsevier Science Ltd
PY  - 2017
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - Nutritional fat is one of the most controversial topics in nutritional research, particularly against the background of obesity. Studies investigating fat taste perception have revealed several associations with sensory, genetic, and personal factors (e.g. BMI). However, neuronal activation patterns, which are known to be highly sensitive to different tastes as well as to BMI differences, have not yet been included in the scheme of fat taste perception. We will therefore provide a comprehensive survey of the sensory, genetic, and personal factors associated with fat taste perception and highlight the benefits of applying neuroimaging research. We will also give a critical overview of studies investigating sensory fat perception and the challenges resulting from multifaceted methodological approaches. In conclusion, we will discuss a multifactorial approach to fat perception to gain a better understanding of the underlying mechanisms that cause varying fat sensitivity which could be responsible for overeating. Such knowledge might be beneficial in new treatment strategies for obesity and overweight.
AU  - Heinze, J.M.
AU  - Preissl, H.
AU  - Fritsche, A.
AU  - Frank, S.*
C1  - 46733
C2  - 37759
SP  - 479-493
TI  - Controversies in fat perception.
JO  - Physiol. Behav.
VL  - 152
IS  - Part B
PY  - 2015
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - Hypothalamic inflammation is a potentially important process in the pathogenesis of high-fat diet-induced metabolic disorders that has recently received significant attention. Microglia are macrophage-like cells of the central nervous system which are activated by pro-inflammatory signals causing local production of specific interleukins and cytokines, and these in turn may further promote systemic metabolic disease. Whether or how this microglial activation can be averted or reversed is unknown. Since running exercise improves systemic metabolic health and has been found to promote neuronal survival as well as the recovery of brain functions after injury, we hypothesized that regular treadmill running may blunt the effect of western diet on hypothalamic inflammation. Using low-density lipoprotein receptor deficient (ldlr-/-) mice to better reflect human lipid metabolism, we first confirmed that microglial activation in the hypothalamus is severely increased upon exposure to a high-fat, or "western", diet. Moderate, but regular, treadmill running exercise markedly decreased hypothalamic inflammation in these mice. Furthermore, the observed decline in microglial activation was associated with an improvement of glucose tolerance. Our findings support the hypothesis that hypothalamic inflammation can be reversed by exercise and suggest that interventions to avert or reverse neuronal damage may offer relevant potential in obesity treatment and prevention.
AU  - Yi, C.-X.
AU  - Al-Massadi, O.*
AU  - Donelan, E.*
AU  - Lehti, M.*
AU  - Weber, J.*
AU  - Ress, C.*
AU  - Trivedi, C.*
AU  - Müller, T.D.
AU  - Woods, S.C.*
AU  - Hofmann, S.M.
C1  - 7481
C2  - 29741
SP  - 485-490
TI  - Exercise protects against high-fat diet-induced hypothalamic inflammation.
JO  - Physiol. Behav.
VL  - 106
IS  - 4
PB  - Elsevier
PY  - 2012
SN  - 0031-9384
ER  - 

TY  - JOUR
AB  - We investigated inbred SWR/J and AKR/J mice, two established models for different susceptibility to diet-induced obesity (DIO), to scrutinize the contribution of physical activity and energy assimilation to the etiology of developing obesity. Body mass gain and body composition of mice fed a high-energy (HE) or a low caloric control diet were monitored. In parallel, assimilated energy, locomotor activity and thermoregulatory behaviour were measured. Activity was continuously registered by radio telemetry and, in addition, Open Field (OF) behaviour was used as a quick screening tool for spontaneous activity before and after the feeding trial. Energy assimilation was increased in both strains on HE (AKR/J: +60.7% and SWR/J: +42.8%) but only in AKR/J, body mass (+8.1%) and fat mass (+40.7%) were significantly elevated. As a trend, total home cage activity was increased and was more scattered in SWR/J. Interestingly, HE stimulated OF activity only in SWR/J in the second trial at the end of the feeding experiment. The spatial pattern of OF activity also differed between strains with obese mice avoiding the core area. Under housing conditions, nest building behaviour was more pronounced in AKR/J. To further evaluate OF behaviour as a marker for spontaneous activity an obese mouse line was investigated. Mice lacking the leptin receptor (db/db) showed already before the onset of obesity lowest activity levels in OF. Adjustment of energy intake, higher activity levels and energy consuming thermoregulatory behaviour are mechanisms employed by SWR/J mice to dissipate excess energy as a defence against the onset of obesity. Therefore our results deciphering mechanisms of DIO-sensitivity in mice contribute to the understanding of inter-individual differences in body weight development in an adipogenic environment.
AU  - Hesse, D.*
AU  - Dunn, M.*
AU  - Heldmaier, G.*
AU  - Klingenspor, M.
AU  - Rozman, J.
C1  - 4274
C2  - 28166
CY  - Oxford
SP  - 370-380
TI  - Behavioural mechanisms affecting energy regulation in mice prone or resistant to diet-induced obesity.
JO  - Physiol. Behav.
VL  - 99
IS  - 3
PB  - Pergamon-Elsevier Sci. Ltd.
PY  - 2010
SN  - 0031-9384
ER  -