People report wanting food when they are hungry, and on eating it they typically report liking the experience. After eating, both wanting and liking decline, but wanting declines to a greater extent, ...which we term the ‘affective discrepancy effect’. In this study we examine the predictors - state, sensory and memory-based - of these affective changes. Hungry participants undertook three tasks: (1) written recollections of what certain foods are like to eat; (2) ratings of wanting and expected flavour liking and fillingness when looking at snacks, and ratings of food and flavour liking when eating them; (3) ratings of bodily state. These tasks were then repeated after lunch. State-based changes in food liking were best predicted by changes in flavour liking. For state-based change in wanting, memory-based information about flavour liking and fillingness from tasks (1) and (2) were all significant predictors. For recollections about eating (task 1), mentions of food fillingness significantly increased pre-to post-lunch and this was the best predictor of the affective discrepancy effect. Recollections of food fillingness are state-dependent, and can arise unbidden (i.e., such recollective content was unprompted). This may reflect one way that memory may selectively influence wanting, and hence whether food intake is initiated or not.
This review focuses on various components of bile acid signaling in relation to cholangiocytes. Their roles as targets for potential therapies for cholangiopathies are also explored. While many ...factors are involved in these complex signaling pathways, this review emphasizes the roles of transmembrane G protein coupled receptor(TGR5), farnesoid X receptor(FXR), ursodeoxycholic acid(UDCA) and the bicarbonate umbrella. Following a general background on cholangiocytes and bile acids,we will expand the review and include sections that are most recently known(within 5–7 years) regarding the field of bile acid signaling and cholangiocyte function. These findings all demonstrate that bile acids influence biliary functions which can, in turn, regulate the cholangiocyte response during pathological events.
Substance P (SP) is involved in the proliferation of cholangiocytes in bile duct–ligated (BDL) mice and human cholangiocarcinoma growth by interacting with the neurokinin‐1 receptor (NK‐1R). To ...identify whether SP regulates liver fibrosis during cholestasis, wild‐type or NK‐1R knockout (NK‐1R–/–) mice that received BDL or sham surgery and multidrug resistance protein 2 knockout (Mdr2–/–) mice treated with either an NK‐1R antagonist (L‐733,060) or saline were used. Additionally, wild‐type mice were treated with SP or saline intraperitoneally. In vivo, there was increased expression of tachykinin precursor 1 (coding SP) and NK‐1R in both BDL and Mdr2–/– mice compared to wild‐type mice. Expression of tachykinin precursor 1 and NK‐1R was significantly higher in liver samples from primary sclerosing cholangitis patients compared to healthy controls. Knockout of NK‐1R decreased BDL‐induced liver fibrosis, and treatment with L‐733,060 resulted in decreased liver fibrosis in Mdr2–/– mice, which was shown by decreased sirius red staining, fibrosis gene and protein expression, and reduced transforming growth factor‐β1 levels in serum and cholangiocyte supernatants. Furthermore, we observed that reduced liver fibrosis in NK‐1R–/– mice with BDL surgery or Mdr2–/– mice treated with L‐733,060 was associated with enhanced cellular senescence of hepatic stellate cells and decreased senescence of cholangiocytes. In vitro, L‐733,060 inhibited SP‐induced expression of fibrotic genes in hepatic stellate cells and cholangiocytes; treatment with L‐733,060 partially reversed the SP‐induced decrease of senescence gene expression in cultured hepatic stellate cells and the SP‐induced increase of senescence‐related gene expression in cultured cholangiocytes. Conclusion: Collectively, our results demonstrate the regulatory effects of the SP/NK‐1R axis on liver fibrosis through changes in cellular senescence during cholestatic liver injury. (Hepatology 2017;66:528–541).
The vicious cycle model of obesity suggests that repeated habitual intake of a diet high in fat and sugar (HFS) results in impairment in hippocampal function which in turn increases impulsive ...behaviours, making it harder to resist unhealthy diet choices. Evidence from studies with rodents consistently show switching to a HFS diet impairs performance on hippocampally-sensitive memory tasks. The limited literature in humans also suggest impaired memory and increased impulsivity related to higher habitual HFS intake. However, these changes in memory and impulsivity have been looked at independently. To investigate how these effects are inter-related, three experiments were conducted where relative HFS intake was related to measures of memory and impulsivity. In Experiment 1 (90 female participants), HFS was associated with higher scores on the Everyday Memory Questionnaire-revised (EMQ), and higher scores on the total, Attention (BISatt) and Motor (BISmot) sub-scales of the Barratt Impulsiveness Scale (BIS11). Experiment 2 (84 women and 35 men), replicated the association between HFS and EMQ, and also found HFS related to poorer performance on the hippocampally-sensitive 4 mountain (4MT) memory task. The association between HFS intake and the BISatt replicated, but there were no significant associations with other BIS11 measures or delay-discounting for monetary rewards. Experiment 3 (199 women and 87 men) replicated the associations between DFS and 4MT and EMQ, and also found an association with overall recall, but not response inhibition, from a Remembering Causes Forgetting task: HFS was also significantly associated with BIS total, BISatt and BISmot. In all three studies these associations remained when potential confounds (BMI, age, gender, hunger state, restrained and disinhibited eating) were controlled for. Mediation analysis found that the effect of HFS on memory at least part mediated the relationship between HFS and impulsivity in Experiments 1 and 3, but not 2. Overall these data provide some support for the vicious cycle model, but also suggest that trait impulsivity may be a risk factor for poor dietary choice.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Liver diseases are perpetuated by the orchestration of hepatocytes and other hepatic non-parenchymal cells. These cells communicate and regulate with each other by secreting mediators such as ...peptides, hormones, and cytokines. Extracellular vesicles (EVs), small particles secreted from cells, contain proteins, DNAs, and RNAs as cargos. EVs have attracted recent research interests since they can communicate information from donor cells to recipient cells thereby regulating physiological events via delivering of specific cargo mediators. Previous studies have demonstrated that liver cells secrete elevated numbers of EVs during diseased conditions, and those EVs are internalized into other liver cells inducing disease-related reactions such as inflammation, angiogenesis, and fibrogenesis. Reactions in recipient cells are caused by proteins and RNAs carried in disease-derived EVs. This review summarizes cell-to-cell communication especially via EVs in the pathogenesis of liver diseases and their potential as a novel therapeutic target.
The development of interoceptive hunger signals Stevenson, Richard J.; Bartlett, Johanna; Wright, Madeline ...
Developmental psychobiology,
March 2023, Letnik:
65, Številka:
2
Journal Article
Recenzirano
Odprti dostop
Hunger is often reported when people experience certain internal sensations (e.g., fatigue) or when they anticipate that a food will be good to eat. The latter results from associative learning, ...while the former was thought to signal an energy deficit. However, energy‐deficit models of hunger are not well supported, so if interoceptive hungers are not “fuel gauges,” what are they? We examined an alternate perspective, where internal states signaling hunger, which are quite diverse, are learned during childhood. A basic prediction from this idea is offspring–caregiver similarity, which should be evident if caregivers teach their child the meaning of internal hunger cues. We tested 111 university student offspring–primary caregiver pairs, by having them complete a survey about their internal hunger states, alongside other information that may moderate this relationship (i.e., gender, body mass index, eating attitudes, and beliefs about hunger). We observed substantial similarity between offspring–caregiver pairs (Cohen's ds from 0.33 to 1.55), with the main moderator being beliefs about an energy‐needs model of hunger, which tended to increase similarity. We discuss whether these findings may also reflect heritable influences, the form that any learning might take, and the implications for child feeding practices.
Interoceptive individual differences have garnered interest because of their relationship with mental health. One type of individual difference that has received little attention is variability in ...the sensation/s that are understood to mean a particular interoceptive state, something that may be especially relevant for hunger. We examined if interoceptive hunger is multidimensional and idiosyncratic, if it is reliable, and if it is linked to dysfunctional eating and beliefs about the causes of hunger. Participants completed a survey just before a main meal, with most retested around 1 month later. We found that interoceptive hunger has 11 dimensions, and while people differ considerably in their combinations of interoceptive hungers, these represent only 4% of all possible permutations. Hunger reports were reliable. We found relationships between variability in hunger interoception and dysfunctional eating, especially for uncontrolled eating. We also found that hunger beliefs were in some cases strongly related to aspects of hunger interoception. The implications of these findings are discussed.
Animals fed a Western-style diet (WS-diet) demonstrate rapid impairments in hippocampal function and poorer appetitive control. We examined if this also occurs in humans. One-hundred and ten healthy ...lean adults were randomized to either a one-week WS-diet intervention or a habitual-diet control group. Measures of hippocampal-dependent learning and memory (HDLM) and of appetitive control were obtained pre- and post-intervention. HDLM was retested at three-week follow-up. Relative to controls, HDLM performance declined in the WS-diet group (
= 0.43), but was not different at follow-up. Appetitive control also declined in the WS-diet group (
= 0.47) and this was strongly correlated with HDLM decline (
= 1.01). These findings demonstrate that a WS-diet can rapidly impair appetitive control in humans-an effect that could promote overeating in consumers of a WS-diet. The study also suggests a functional role for the hippocampus in appetitive control and provides new evidence for the adverse neurocognitive effects of a WS-diet.
Drinking sugar-sweetened beverages (SSBs) seems to uniquely contribute to excess weight gain, and several mechanisms have been proposed to account for this. Here we examine a further proposal, namely ...that explicit wanting and liking for SSBs may be less sensitive to changes in physiological state, when contrasted to equi-palatable solid sweet snacks. Study 1 explored this by having participants rate wanting for (on seeing) and liking of (on tasting) several SSBs and snacks, before and after receiving a solid lunch with ad libitum water. Participant reports of hunger and thirst, obtained at multiple time-points, equally reduced across lunch. Wanting for the snacks decreased significantly more across lunch than liking, but for the SSBs, wanting and liking decreased in parallel. Study 2 engineered a far more dramatic alteration in thirst, by using fluid deprivation, a liquid lunch, and encouraging drinking to satiation. This time, reduction in thirst exceeded reduction in hunger. However, all this served to achieve was an equivalent change across lunch for snacks and SSBs, with wanting reducing more than liking now for both. These findings suggest that changes in wanting, relative to liking, for SSBs, are less sensitive to alterations in physiological state than equi-palatable solid snacks, enhancing the chance of consumption.
Background and Aims
Nonalcoholic fatty liver disease (NAFLD) is simple steatosis but can develop into nonalcoholic steatohepatitis (NASH), characterized by liver inflammation, fibrosis, and ...microvesicular steatosis. Mast cells (MCs) infiltrate the liver during cholestasis and promote ductular reaction (DR), biliary senescence, and liver fibrosis. We aimed to determine the effects of MC depletion during NAFLD/NASH.
Approach and Results
Wild‐type (WT) and KitW‐sh (MC‐deficient) mice were fed a control diet (CD) or a Western diet (WD) for 16 weeks; select WT and KitW‐sh WD mice received tail vein injections of MCs 2 times per week for 2 weeks prior to sacrifice. Human samples were collected from normal, NAFLD, or NASH mice. Cholangiocytes from WT WD mice and human NASH have increased insulin‐like growth factor 1 expression that promotes MC migration/activation. Enhanced MC presence was noted in WT WD mice and human NASH, along with increased DR. WT WD mice had significantly increased steatosis, DR/biliary senescence, inflammation, liver fibrosis, and angiogenesis compared to WT CD mice, which was significantly reduced in KitW‐sh WD mice. Loss of MCs prominently reduced microvesicular steatosis in zone 1 hepatocytes. MC injection promoted WD‐induced biliary and liver damage and specifically up‐regulated microvesicular steatosis in zone 1 hepatocytes. Aldehyde dehydrogenase 1 family, member A3 (ALDH1A3) expression is reduced in WT WD mice and human NASH but increased in KitW‐sh WD mice. MicroRNA 144‐3 prime (miR‐144‐3p) expression was increased in WT WD mice and human NASH but reduced in KitW‐sh WD mice and was found to target ALDH1A3.
Conclusions
MCs promote WD‐induced biliary and liver damage and may promote microvesicular steatosis development during NAFLD progression to NASH through miR‐144‐3p/ALDH1A3 signaling. Inhibition of MC activation may be a therapeutic option for NAFLD/NASH treatment.
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