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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The multiplicity of proposed mechanisms for obesity is confusing and many questions remain to be answered. A review of all the proposed mechanisms for obesity suggests that they can be placed in two groups (Table 3). The first centres on the role of the hypothalamus in the regulation of body weight. With further knowledge it may be possible to find unifying mechanisms originating in the brain for the set-point theory, the autonomic nervous system imbalance hypothesis, the thermogenesis, hyperphagia and the hyperinsulinaemia hypotheses and the gestational undernutrition hypothesis. This group of mechanisms suggests that obesity is due to altered function of central regulatory mechanisms and that the various related hypotheses are merely looking at different aspects of the same problem. The second centres on abnormalities intrinsic to the adipocyte and could link the fat cell and perinatal overnutrition theories. This group of theories suggests that an abnormality at the fat cell level, either genetic or acquired, can result in the excessive accumulation of fat. The two groups are not contradictory. The ability to develop obesity as a result of a fat cell abnormality does not negate the existence of regulatory central mechanisms since there is a finite capacity for these mechanisms to operate.
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PMID:Animal models of obesity--theories of aetiology. 798 Mar 45

Cholecystokinin (CCK) is suggested to be involved, e.g. in the central nervous modulation of food intake, possibly by acting within specific hypothalamic nuclei. Perinatal overnutrition predisposes to permanent obesity and hyperphagia, while underlying mechanisms are unclear. By reducing the litter size from the 3rd to 21st day of life, early overnutrition was induced in newborn rats. At weaning, clear overweight (P < 0.001), hyperglycaemia (P < 0.05), hyperinsulinaemia (P < 0.001), and insulin resistance (P < 0.001) occured. These early signs of obesity were associated with a significantly decreased number of CCK-positive neurons in the paraventricular hypothalamic nucleus (P < 0.002). In conclusion, due to neonatal overfeeding malformation of CCKergic neurons at the end of the critical hypothalamic differentiation period occurs. Long-term consequences on CCK-related neuroendocrine regulations could be suggested, including those affecting food intake and body weight gain.
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PMID:Reduction of cholecystokinin-8S-neurons in the paraventricular hypothalamic nucleus of neonatally overfed weanling rats. 987 40

Overnutrition during critical developmental periods is suggested to be a risk factor for obesity and associated metabolic disorders in later life. Underlying mechanisms are unknown. Neuropeptides are essentially involved in the central nervous regulation of body weight. For instance, hypothalamic galanin (GAL) is a stimulator of food intake and body weight gain. To investigate long-term consequences of early postnatal overfeeding, the normal litter size of Wistar rats (n=10; controls) was reduced from day 3 to day 21 of life to only 3 pups per mother (small litters, SL; overnutrition). Throughout life, SL rats displayed hyperphagia (p<0.01), overweight (p<0.0001), hyperinsulinemia (p<0.01), impaired glucose tolerance (p<0.001), elevated triglycerides (p<0.001), and an increased systolic blood pressure (p<0.05). In adulthood, an increase of GAL-neurons in the arcuate hypothalamic nucleus (ARC) was found (p<0.001), positively correlated to body weight (p<0.001). A second experiment revealed hyperinsulinemia (p<0.001) and increased hypothalamic insulin levels (p<0.05) in SL rats during early postnatal life. Already on day 21 of life, i.e., at the end of the critical hypothalamic differentiation period, in SL rats the number of GAL-neurons was increased in the ARC (p<0.001), showing a positive correlation to body weight and insulin (p<0.05). In conclusion, neonatally acquired persisting malformation of hypothalamic galaninergic neurons, induced by early overfeeding and hyperinsulinism, might promote the development of overweight and syndrome X-like alterations during life.
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PMID:Perinatal elevation of hypothalamic insulin, acquired malformation of hypothalamic galaninergic neurons, and syndrome x-like alterations in adulthood of neonatally overfed rats. 1041 13

Social circumstances often impinge on later generations in a socio-economic manner, giving children an uneven start in life. Overfeeding and overeating might not be an exception. The pathways might be complex but one direct mechanism could be genomic imprinting and loss of imprinting. An intergenerational "feedforward" control loop has been proposed, that links grandparental nutrition with the grandchild's growth. The mechanism has been speculated to be a specific response, e.g. to their nutritional state, directly modifying the setting of the gametic imprint on one or more genes. This study raises the question: Can overnutrition during a child's slow growth period trigger such direct mechanisms and partly determine mortality? Data were collected by following-up a cohort born in 1905 in Overkalix parish, northernmost Sweden. The probands were characterised by their parents' or grandparents' access to food during their own slow growth period. Availability of food in the area was defined by referring to historical data on harvests and food prices, records of local community meetings and general historical facts. If there was a surfeit of food in the environment when the paternal grandfather was a 9-12 year old boy a shortening of the proband survival could be demonstrated. The influence of parents', maternal grandparents' and paternal grandmothers' access to food during their slow growth period was discounted in a multivariable analysis. The results are indicative of very early programming mechanisms in human adaptation to the social environment.
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PMID:Longevity determined by paternal ancestors' nutrition during their slow growth period. 1136 78

During the period from October 1, 1999 till February 29, 2000, 500 pregnant women were analyzed according to overnutrition, i.e. weight gain. The analysis was performed in the Department of Gynecology and Obstetrics, Osijek University Hospital for pregnant women from east Slavonia, Baranya and west Srijem, where large quantities of dietary fats and carbohydrates are used. The mean weight gain during pregnancy was assessed. The mean weight of male infants in primiparae was 3.22 g, i.e. 8% higher than the mean value for the same population in Zagreb. The rate of EPH gestoses in patients with weight gain over 12 kg was significantly higher (4.0%) than in those with weight gain less than 12 kg (1.8%). In pregnant patients with weight gain > 12 kg, the rate of cesarean section was significantly higher (9.2%) than in those with weight gain < 12 kg (4.4% o). Perinatal mortality was significantly higher (10.0%) in pregnancies with weight gain > 12 kg than in those with weight gain < 12 kg (2.0% o). It is concluded that dependence on overeating in pregnancy may result in higher rates of EPH gestosis, cesarean section and perinatal mortality.
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PMID:Maternal overnutrition and pregnancy. 1245 52

The hypothalamic regulatory system of body weight which develops in rats during critical periods of early postnatal life seems to express plastic changes depending on nutrition at that time. Adult rats previously exposed to early postnatal overnutrition by raising them in small litters become persistently predisposed to overweight, hyperphagia and hyperleptinaemia. The hypothesis was raised that feeding-related peptides could be involved through altered effects on neuronal activity of the regulatory systems of such rats. This was studied on brain slices of small-litter rats and normal-weight controls between days 60 and 120 of life. Neurons of the medial parvocellular part of the paraventricular nucleus were significantly activated by the adiposity signals leptin, insulin and amylin in controls. This is a kind of negative feedback, because activation of these neurons is known to be followed in vivo by increased energy expenditure. GABAergic mechanisms seem to affect these neuronal responses because the activating effects of insulin and amylin were reduced in the presence of a GABA(A) receptor antagonist. In overweight small-litter rats, however, the neuronal responses to the adiposity signals were significantly changed; activating effects were reduced and inhibitory effects increased. By means of blockade of GABA(A) receptors, significant alterations in the neuronal responses to leptin, insulin and amylin in small-litter rats were prevented. Responses to the peptides were reversed and now resembled those of controls. In conclusion, changes in neuronal wiring with GABAergic interneurons seem to contribute to a persistently reduced negative feedback of adiposity signals in early postnatally overfed rats.
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PMID:GABAA receptor antagonists prevent abnormalities in leptin, insulin and amylin actions on paraventricular hypothalamic neurons of overweight rats. 1655 87

The North American epidemic of overeating, combined with a sedentary lifestyle, has led to a growing prevalence of obesity, diabetes, and the "metabolic syndrome" in children. Excessive caloric intake does not imply adequate nutrition, and vitamin-deficiency syndromes still occur in some American children. Here we describe cases of scurvy and vitamin D deficiency in 2 children with cognitive disorders. Thorough dietary histories suggested the diagnosis in each patient and, had they been obtained at presentation, would likely have obviated invasive diagnostic workup, unnecessary stress to the patients and their families, and significant functional disability. Overnutrition and malnutrition may coexist, particularly among those with abnormal cognition or autistic spectrum disorders. Classic nutritional deficiencies must not be omitted from the differential diagnosis. A comprehensive dietary history and screening for vitamin deficiencies in at-risk children are important aspects of preventive health care and are essential for prompt diagnosis and treatment.
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PMID:Scurvy and rickets masked by chronic neurologic illness: revisiting "psychologic malnutrition". 1733 93

Experimental and clinical studies have demonstrated that early postnatal overnutrition represents a risk factor for later obesity and associated metabolic and cardiovascular disturbance. In the present study, we assessed the levels of glucose transporter 4 (GLUT-4), GLUT-1, insulin receptor (IR), IR substrate 1 (IRS-1), phosphatidylinositol 3-kinase (PI3K) and Akt expression, as well as insulin-stimulated glucose transport and Akt activity in adipocytes from adult rats previously raised in small litters (SL). The normal litter (NL) served as control group. We also investigated glycemia, insulinemia, plasma lipid levels, and glucose tolerance. Our data demonstrated that early postnatal overfeeding induced a persistent hyperphagia accompanied by a significant increase in body weight until 90 days of age. The SL group also presented a significant increase ( approximately 42%) in epidydimal fat weight. Blood glucose, plasma insulin, and lipid levels were similar among the animals from the SL and NL groups. While insulin-stimulated glucose uptake was approximately twofold higher in adipocytes from the NL group, no stimulatory effect was observed in the SL group. The impaired insulin-stimulated glucose transport in adipose cells from the SL rats was associated with a significant decrease in GLUT-4, IRS-1 and PI3K expression, and Akt activity. In contrast, IR and Akt expression in adipocytes was not different between the SL and NL groups. Despite these alterations, our results showed no differences in glucose tolerance test in rats raised under different feeding conditions. Our findings reinforce a potent and long-term effect of neonatal overfeeding, which can program major changes in the metabolic regulatory mechanisms.
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PMID:Low expression of insulin signaling molecules impairs glucose uptake in adipocytes after early overnutrition. 1800 Mar 10

Postnatal early overnutrition (EO) is a risk factor for obesity in adult life. Rats raised in a small litter can develop hyperinsulinaemia, hyperphagia, hyperleptinaemia and hypertension as adults. Since leptin regulates the hypothalamic-pituitary-thyroid axis and the metabolism of thyroid hormones, we studied the leptin signalling pathway in pituitary and thyroid glands of the postnatal EO model. To induce EO, at the third day of lactation the litter size was reduced to three pups per litter (SL group). In control litters (NL group), the litter size was adjusted to 10 pups per litter. Body weight and food intake were monitored. Rat offspring were killed at 21 (weaning) and 180 days old (adulthood). Plasma thyroid hormones, thyroid-stimulating hormone (TSH) and leptin were measured by radioimmunoassay. Proteins of the leptin signalling pathway were analysed by Western blotting. Body weight of offspring in the SL group was higher from the seventh day of lactation (+33%, P < 0.05) until 180 days old (+18%, P < 0.05). Offspring in the SL group showed higher visceral fat mass at 21 and 180 days old (+176 and +52%, respectively, P < 0.05), but plasma leptin was higher only at 21 days (+88%, P < 0.05). The SL offspring showed higher plasma TSH, 3,5,3'-triiodothronine (T(3)) and thyroxine (T(4)) at 21 days (+60, +91 and +68%, respectively, P < 0.05), while the opposite was observed at 180 days regarding thyroid hormones (T(3), -10%; and T(4), -30%, P < 0.05), with no difference in TSH levels. In hypothalamus, no change was observed in the leptin signalling pathway at 21 days. However, lower janus thyrosine kinase 2 (JAK2) and phosphorilated-signal transducer and activator of transcription-3 (p-STAT3) content were detected in adulthood. In pituitary, the SL group presented higher leptin receptors (Ob-R), JAK2 and p-STAT3 content at 21 days and lower JAK2 and STAT3 content at 180 days old. In contrast, in thyroid, the Ob-R expression was lower in young SL rats, while the adult SL group presented higher Ob-R and JAK2 content. We showed that postnatal EO induces short- and long-term effects upon the hypothalamic-pituitary-thyroid axis. These changes may help to explain future development of metabolic and endocrine dysfunctions, such as metabolic syndrome and hypothyroidism.
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PMID:Postnatal early overnutrition changes the leptin signalling pathway in the hypothalamic-pituitary-thyroid axis of young and adult rats. 1948 48

Altered nutritional experiences such as undernutrition, overnutrition, and modified milk formula in the immediate postnatal life via the phenomenon of metabolic programming have been identified as one of the components in the etiology of metabolic syndrome. We have developed a rat model in which an altered dietary experience in the form of a high-carbohydrate (HC) milk formula in the immediate postnatal life of rat pups results in chronic hyperinsulinemia and adult-onset obesity in these rats. The HC dietary modification causes functional alterations in pancreatic islets and the hypothalamus during the period of the dietary modification. These early adaptations in islets (supporting hyperinsulinemia) and the hypothalamus (supporting hyperphagia and increased body weight gain) persist in the postweaning period despite withdrawal of the HC milk formula at the time of weaning. In female rat pups receiving the HC milk formula, metabolic programming effects translate into an adverse (hyperinsulinemic, hyperleptinemic, and obese) intrauterine environment during pregnancy, causing spontaneous transfer of the maternal phenotype to the progeny (generational effect). Our results suggest that alterations in feeding practices for babies (early introduction of cereals, fruits, etc.) and babies born to obese/hyperinsulinemic mothers may be contributing factors for the obesity epidemic prevalent in developed and developing countries.
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PMID:Metabolic programming due to alterations in nutrition in the immediate postnatal period. 2010 49


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