The hypothalamus, hormones, and hunger: alterations in human obesity and illness

Goldstone, Anthony P.

doi:10.1016/s0079-6123(06)53003-1

Cited by 66 publications

(43 citation statements)

References 113 publications

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“…Haig and Wharton (2003) describe how the complacent nature of Prader-Willi infants (with low levels of crying and wakefulness), and their compulsive self-foraging for food after the usual age of weaning, can be interpreted in the context of reduced demands on mothers, as expected under imprinted-gene biases involving loss of paternal-gene expression. Prader-Willi syndrome is known to centrally-involve hypothalamic alterations and relatively low levels of oxytocin (Swaab et al 1995;Holland et al 2003;Hoybye 2004;Goldstone 2006), which is consistent with the oxytocin-reducing effects of Ndn gene knockouts in mice ) and the expected behavioral effects of lower oxytocin levels -reduced motivation towards social bonding behavior. These considerations suggest that Prader-Willi syndrome should involve insecure attachment in children, especially among cases due to maternal uniparental disomy where the genomic deviations towards maternal imprinted-gene effects are more extensive.…”

Section: Noted: "In Dealing Here With the Embryology Of The Human Minmentioning

confidence: 75%

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

Crespi

2011

Brain, Behavior and Epigenetics

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I describe and evaluate the hypothesis that effects from parent-offspring conflict and genomic imprinting on human neurodevelopment and behavior are central to evolved systems of mother-child attachment. The psychological constructs of Bowlby's attachment theory provide phenomenological descriptions of how attachment orchestrates affective-cognitive development, and patterns of imprinted gene expression and co-expression provide evidence of epigenetic and evolutionary underpinnings to human growth and neurodevelopment. Social-environmental perturbations to the development of normally-secure attachment, and alterations to evolved systems of parent-offspring conflict and imprinted-gene effects, are expected to lead to specific forms of maladaptation, manifest in psychiatric conditions affecting social-brain development. In particular, under-development of the social brain in autism may be mediated in part by mechanisms that lead to physically enhanced yet psychologically under-developed attachment to the mother, and affective-psychotic conditions, such as schizophrenia and depression, may be mediated in part by forms of insecure attachment and by increased relative effects of the maternal brain, both directly from mothers and via imprinted-gene effects in offspring. These hypotheses are concordant with findings from epidemiology, attachment theory, psychiatry, and genetic and epigenetic analyses of risk factors for autism and affective-psychotic conditions, they make novel predictions for explaining the causes of psychosis in Prader-Willi syndrome and idiopathic schizophrenia, and they suggest avenues for therapeutic interventions based on normalizing alterations to epigenetic networks and targeting public-health interventions towards reduction of perturbations to the development of secure attachment in early childhood and individuation during adolescence.

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Section: Noted: "In Dealing Here With the Embryology Of The Human Minmentioning

confidence: 75%

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

Crespi

2011

Brain, Behavior and Epigenetics

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“…Pancreatic polypeptide Previous studies have found that, compared with non-obese and obese controls, fasting levels of PP are either normal 22,23,45 or decreased, 10,21,35 and post-prandial levels decreased, 10,21 --23,35,45 in both children over the age of 5 --7 years and adults with PWS. Although eating behaviour was rarely described in the non-adult studies, most of the children did have marked obesity.…”

Section: Discussionmentioning

confidence: 99%

“…45 Post-prandial PYY levels have generally been found to be normal in PWS children and adults, 38,41,44 though one study found decreased post-prandial levels. 43 Similarly fasting plasma levels of the anorexigenic gut hormone GLP-1 that is cosecreted from intestinal L-cells with PYY appear normal in PWS children and adults, 10,34,38,48 and post-prandial GLP-1 levels are normal in PWS adults PWS. 10,38 Fasting and post-prandial plasma levels of CCK 11,23,25,41 and GIP, 21,38,45 other gut hormones involved in appetite regulation and glucose homeostasis, also appear normal in PWS children (over 7 --11 years) or adults.…”

Section: Ghrelinmentioning

confidence: 97%

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Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

et al. 2012

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OBJECTIVE: Prader --Willi syndrome (PWS) is a genetic neurodevelopmental disorder with several nutritional phases during childhood proceeding from poor feeding, through normal eating without and with obesity, to hyperphagia and life-threatening obesity, with variable ages of onset. We investigated whether differences in appetite hormones may explain the development of abnormal eating behaviour in young children with PWS. SUBJECTS: In this cross-sectional study, children with PWS (n ¼ 42) and controls (n ¼ 9) aged 7 months --5 years were recruited. Mothers were interviewed regarding eating behaviour, and body mass index (BMI) was calculated. Fasting plasma samples were assayed for insulin, leptin, glucose, peptide YY (PYY), ghrelin and pancreatic polypeptide (PP). RESULTS: There was no significant relationship between eating behaviour in PWS subjects and the levels of any hormones or insulin resistance, independent of age. Fasting plasma leptin levels were significantly higher (mean±s.d.: 22.6±12.5 vs 1.97 ± 0.79 ng ml À1 , P ¼ 0.005), and PP levels were significantly lower (22.6 ± 12.5 vs 69.8 ± 43.8 pmol l À1 , Po0.001) in the PWS group compared with the controls, and this was independent of age, BMI, insulin resistance or IGF-1 levels. However, there was no significant difference in plasma insulin, insulin resistance or ghrelin levels between groups, though PYY declined more rapidly with age but not BMI in PWS subjects. CONCLUSION: Even under the age of 5 years, PWS is associated with low levels of anorexigenic PP, as in older children and adults. Hyperghrelinaemia or hypoinsulinaemia was not seen in these young children with PWS. Change in these appetite hormones was not associated with the timing of the transition to the characteristic hyperphagic phase. However, abnormal and/or delayed development or sensitivity of the effector pathways of these appetitive hormones (for example, parasympathetic and central nervous system) may interact with low PP levels, and later hyperghrelinaemia or hypoinsulinaemia, to contribute to hyperphagia in PWS.

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“…NPY is widely distributed within vertebrate species as its presence in the brain and role in stimulating food intake has been confirmed in various vertebrates from fish to humans (Allen et al, 1983;Crespi, Vaudry, and Denver, 2004;Goldstone, 2006;Grove, Chen, Koegler, Schiffmaker, Susan Smith, and Cameron, 2003;Inui, Okita, Nakajima, Inoue, Sakatani, Oya, Morioka, Okimura, Chihara, and Baba, 1991;Kuenzel, Douglass, and Davison, 1987;Morley, Hernandez, and Flood, 1987;Volkoff, Canosa, Unniappan, Cerda-Reverter, Bernier, Kelly, and Peter, 2005). While the function of NPY has been extensively studied in a few temperate zone mammals, to our knowledge no data have been collected in tropical or semi-tropical mammals which have less predictable food supplies and as such may have differences in neuropeptide regulation of appetite and feeding.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y influences acute food intake and energy status affects NPY immunoreactivity in the female musk shrew (Suncus murinus)

Bojkowska

Hamczyk

Tsai

et al. 2008

Hormones and Behavior

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Neuropeptide Y (NPY) stimulates feeding, depresses sexual behavior, and its expression in the brain is modulated by energetic status. We examined the role of NPY in female musk shrews, a species with high energetic and reproductive demands; they store little fat, and small changes in energy can rapidly diminish or enhance sexual receptivity. Intracerebroventricular infusion of NPY enhanced acute food intake in shrews, however, NPY had little affect on sexual receptivity. The distribution of NPY immunoreactivity in the female musk shrew brain was unremarkable, but energy status differentially affected NPY immunoreactivity in several regions. Similar to what has been noted in other species, NPY immunoreactivity was less dense in brains of ad libitum shrews and greater in shrews subjected to food restriction. In two midbrain regions, both of which contain high levels of gonadotropin releasing hormone II (GnRH II) which has anorexigenic actions in shrews, NPY immunoreactivity was more sensitive to changes in food intake. In these regions, acute refeeding (90-180 minutes) after food restriction reduced NPY immunoreactivity to levels noted in ad libitum shrews. We hypothesize that interactions between NPY and GnRH II maintain energy homeostasis and reproduction in the musk shrew.

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The hypothalamus, hormones, and hunger: alterations in human obesity and illness

Cited by 66 publications

References 113 publications

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

Neuropeptide Y influences acute food intake and energy status affects NPY immunoreactivity in the female musk shrew (Suncus murinus)

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