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Postnatal weight gain modifies severity and functional outcome of oxygen-induced proliferative retinopathy

Stahl, Andreas (författare)
Chen, Jing (författare)
Sapieha, Przemyslaw (författare)
visa fler...
Seaward, Molly R (författare)
Krah, Nathan M (författare)
Dennison, Roberta J (författare)
Favazza, Tara (författare)
Bucher, Felicitas (författare)
Löfqvist, Chatarina (författare)
Ong, Huy (författare)
Hellström, Ann, 1959- (författare)
Göteborgs universitet, Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering, University of Gothenburg, Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Chemtob, Sylvain (författare)
Akula, James D (författare)
Smith, Lois E H (författare)
visa färre...
Göteborgs universitet Sahlgrenska akademin. Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering. 
2010
Engelska.
Ingår i: The American journal of pathology. - 1525-2191. ; 177:6, s. 2715
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • In clinical studies, postnatal weight gain is strongly associated with retinopathy of prematurity (ROP). However, animal studies are needed to investigate the pathophysiological mechanisms of how postnatal weight gain affects the severity of ROP. In the present study, we identify nutritional supply as one potent parameter that affects the extent of retinopathy in mice with identical birth weights and the same genetic background. Wild-type pups with poor postnatal nutrition and poor weight gain (PWG) exhibit a remarkably prolonged phase of retinopathy compared to medium weight gain or extensive weight gain pups. A high (r(2) = 0.83) parabolic association between postnatal weight gain and oxygen-induced retinopathy severity is observed, as is a significantly prolonged phase of proliferative retinopathy in PWG pups (20 days) compared with extensive weight gain pups (6 days). The extended retinopathy is concomitant with prolonged overexpression of retinal vascular endothelial growth factor in PWG pups. Importantly, PWG pups show low serum levels of nonfasting glucose, insulin, and insulin-like growth factor-1 as well as high levels of ghrelin in the early postoxygen-induced retinopathy phase, a combination indicative of poor metabolic supply. These differences translate into visual deficits in adult PWG mice, as demonstrated by impaired bipolar and proximal neuronal function. Together, these results provide evidence for a pathophysiological correlation between poor postnatal nutritional supply, slow weight gain, prolonged retinal vascular endothelial growth factor overexpression, protracted retinopathy, and reduced final visual outcome.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Oftalmologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Ophthalmology (hsv//eng)

Nyckelord

Oftalmologi
Ophtalmology
Age Factors
Animals
Animals
Newborn
Disease Models
Animal
Humans
Infant
Newborn
Mice
Mice
Inbred C57BL
Oxygen
adverse effects
Oxygen Inhalation Therapy
adverse effects
Parturition
physiology
Prognosis
Retina
metabolism
Retinopathy of Prematurity
diagnosis
etiology
genetics
pathology
Severity of Illness Index
Vascular Endothelial Growth Factor A
genetics
metabolism
Weight Gain
physiology

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