FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1935576158> ?p ?o ?g. }

• W1935576158 abstract "Rapid weight gain after birth is associated with increased risk of metabolic disease in adulthood. This metabolic malprogramming may be mediated by endocrine disturbances during critical periods of development. Several hormones that act on hypothalamic feeding circuits in adulthood to regulate energy homeostasis, such as leptin and ghrelin, are also involved in the postnatal development of these circuits. Previous studies have shown that leptin promotes the growth of axons from the arcuate nucleus of the hypothalamus(ARH), whereas ghrelin inhibits arcuate axon growth. The aim of this thesis was to study whether accelerated growth during early postnatal life is associated with alterations in the ghrelin and leptin systems during postnatal development. Our general objective was also to examine the relative contribution of ghrelin and leptin in the metabolic malprogramming associated with neonatal overnutrition. To manipulate nutrient intake specifically during postnatal (pre-weaning) life, we manipulated litter size on postnatal day 3 by randomly distributing pups among mothers such that small litters (overfed) had 3 pups and normal litters (normal fed) had 7 pups. SL pups gained substantially more weight than NL pups during lactation, and remained overweight throughout adulthood on a standard chow diet. Adult SL mice displayed increased adiposity and and elevated fasting glucose levels. Adult SL mice also gained more weight and fat when exposed to an obesogenic diet. During postnatal development, SL pups displayed reduced total and active circulating ghrelin levels compared to NL pups, particularly during the third week postnatal week. This was associated with decreased stomach expression of ghrelin in the third postnatal week. Normalization of hypoghrelinemia in overnourished pups is relatively ineffective in ameliorating metabolic outcomes, suggesting that SL pups may present ghrelin resistance. Consistent with this idea, pups raised in small litters displayed an impaired central response to peripheral ghrelin. The mechanisms underlying this ghrelin resistance include diminished ghrelin transport into the brain.In addition to marked changes in ghrelin levels, neonatally overnourished pups also display a marked increase in circulating leptin levels during early postnatal life. To investigate whether these abnormally high levels in circulating leptin levels might be causally involved in the central leptin resistance and metabolic programming, we used a competitive leptin antagonist to partially block leptin action in SL and NL mice between P6 and 16, i.e. when when endogenous leptin levels are high in SL mice. Neonatal injection of the leptin antagonist had no effect on postnatal growth or adult body weight. However, SL pups treated with the leptin antagonist displayed a marked reduction in adult fat mass and normalized glucose tolerance and insulin sensitivity. Previous studies reported that SL exhibit early central leptin resistance. Remarkably, pretreatment with leptin antagonist significantly increased leptin-induced pSTAT3 levels in the ARH of SL pups, suggesting that neonatal leptin antagonism may normalize metabolic programming in neonatally overnourished mice by enhancing central leptin sensitivity. Together our data show that early postnatal nutrition influence the pattern of secretion of metabolic hormones and their ability to act on hypothalamic regions involved in appetite regulation. These hormonal alterations may contribute to the metabolic defects observed in subject exposed to overnutrition during early life." @default.
• W1935576158 created "2016-06-24" @default.
• W1935576158 creator A5002008461 @default.
• W1935576158 date "2014-11-26" @default.
• W1935576158 modified "2023-09-27" @default.
• W1935576158 title "Nutritional regulation of metabolic hormones implicated in the postnatal programming of obesity : the case of leptin and ghrelin" @default.
• W1935576158 cites W1996713062 @default.
• W1935576158 cites W2144489715 @default.
• W1935576158 hasPublicationYear "2014" @default.
• W1935576158 type Work @default.
• W1935576158 sameAs 1935576158 @default.
• W1935576158 citedByCount "0" @default.
• W1935576158 crossrefType "dissertation" @default.
• W1935576158 hasAuthorship W1935576158A5002008461 @default.
• W1935576158 hasConcept C112672928 @default.
• W1935576158 hasConcept C126322002 @default.
• W1935576158 hasConcept C134018914 @default.
• W1935576158 hasConcept C2491326 @default.
• W1935576158 hasConcept C2776659692 @default.
• W1935576158 hasConcept C2777003273 @default.
• W1935576158 hasConcept C2778302649 @default.
• W1935576158 hasConcept C2779234561 @default.
• W1935576158 hasConcept C2779357093 @default.
• W1935576158 hasConcept C2780613262 @default.
• W1935576158 hasConcept C2780655333 @default.
• W1935576158 hasConcept C511355011 @default.
• W1935576158 hasConcept C54355233 @default.
• W1935576158 hasConcept C71315377 @default.
• W1935576158 hasConcept C71924100 @default.
• W1935576158 hasConcept C86803240 @default.
• W1935576158 hasConceptScore W1935576158C112672928 @default.
• W1935576158 hasConceptScore W1935576158C126322002 @default.
• W1935576158 hasConceptScore W1935576158C134018914 @default.
• W1935576158 hasConceptScore W1935576158C2491326 @default.
• W1935576158 hasConceptScore W1935576158C2776659692 @default.
• W1935576158 hasConceptScore W1935576158C2777003273 @default.
• W1935576158 hasConceptScore W1935576158C2778302649 @default.
• W1935576158 hasConceptScore W1935576158C2779234561 @default.
• W1935576158 hasConceptScore W1935576158C2779357093 @default.
• W1935576158 hasConceptScore W1935576158C2780613262 @default.
• W1935576158 hasConceptScore W1935576158C2780655333 @default.
• W1935576158 hasConceptScore W1935576158C511355011 @default.
• W1935576158 hasConceptScore W1935576158C54355233 @default.
• W1935576158 hasConceptScore W1935576158C71315377 @default.
• W1935576158 hasConceptScore W1935576158C71924100 @default.
• W1935576158 hasConceptScore W1935576158C86803240 @default.
• W1935576158 hasOpenAccess W1935576158 @default.
• W1935576158 hasRelatedWork W1226057016 @default.
• W1935576158 hasRelatedWork W1507740248 @default.
• W1935576158 hasRelatedWork W2003342987 @default.
• W1935576158 hasRelatedWork W2004309233 @default.
• W1935576158 hasRelatedWork W2028861833 @default.
• W1935576158 hasRelatedWork W2042943427 @default.
• W1935576158 hasRelatedWork W2048533645 @default.
• W1935576158 hasRelatedWork W2059513542 @default.
• W1935576158 hasRelatedWork W2062316965 @default.
• W1935576158 hasRelatedWork W2073224049 @default.
• W1935576158 hasRelatedWork W2090091066 @default.
• W1935576158 hasRelatedWork W2235605063 @default.
• W1935576158 hasRelatedWork W2516390136 @default.
• W1935576158 hasRelatedWork W2533975026 @default.
• W1935576158 hasRelatedWork W2608489327 @default.
• W1935576158 hasRelatedWork W2794968146 @default.
• W1935576158 hasRelatedWork W2970593656 @default.
• W1935576158 hasRelatedWork W2997741069 @default.
• W1935576158 hasRelatedWork W2997830134 @default.
• W1935576158 hasRelatedWork W3161651288 @default.
• W1935576158 isParatext "false" @default.
• W1935576158 isRetracted "false" @default.
• W1935576158 magId "1935576158" @default.
• W1935576158 workType "dissertation" @default.