Literature DB >> 9450849

Comparison of leptin protein levels in Prader-Willi syndrome and control individuals.

M G Butler1, J Moore, A Morawiecki, M Nicolson.   

Abstract

Prader-Willi syndrome (PWS) is characterized by early childhood obesity, mental deficiency, hypogonadism, hypotonia, hypopigmentation, short stature, small hands and feet, and a characteristic face. It is the most common genetic cause of obesity and obesity is the most significant health problem for PWS patients. Ob protein (leptin), which is produced by adipose tissue, is thought to play a significant role in obesity; thus, unusually low plasma leptin levels, or relative loss of sensitivity to leptin in PWS subjects, could be an important factor in their obesity. We measured plasma leptin levels in 19 obese and 14 non-obese PWS patients [mean body mass index (BMI) 37.2 and 22.0, respectively] and compared these levels to those of 28 obese controls (mean BMI 35.5) and 16 non-obese control individuals (mean BMI 21.6). The mean plasma leptin concentration (ng/ml) for obese PWS subjects was 33.4 and 23.6 for non-obese PWS subjects. Obese control leptin was 36.2 ng/ml and non-obese control was 9.9. Among the control groups, leptin levels in females were significantly higher than those in males; the obese males and females had significantly higher leptin than their respective non-obese counterparts. These differences did not hold true for the PWS subjects. Leptin levels in obese PWS males and females were similar, and the same was true of the non-obese PWS males and females. The differences between obese and non-obese PWS subjects of both sexes were small and not significant. Comparing control groups with their PWS counterparts revealed no significant differences, with one exception: circulating plasma leptin levels in non-obese PWS males were nearly five times higher than in non-obese control males with similar BMI. This difference may reflect a more female pattern of fat distribution and hypogonadism, which are characteristic of PWS males. Leptin levels in PWS patients were not obviously correlated with the chromosome 15 finding seen in the patients.

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Year:  1998        PMID: 9450849      PMCID: PMC6775636     

Source DB:  PubMed          Journal:  Am J Med Genet        ISSN: 0148-7299


  23 in total

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Authors:  James O Hill; Mary Kaler; Bennett Spetalnick; George Reed; Merlin G Butler
Journal:  Dysmorphol Clin Genet       Date:  1990

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Authors:  M Maffei; J Halaas; E Ravussin; R E Pratley; G H Lee; Y Zhang; H Fei; S Kim; R Lallone; S Ranganathan
Journal:  Nat Med       Date:  1995-11       Impact factor: 53.440

6.  Prader-Willi syndrome: current understanding of cause and diagnosis.

Authors:  M G Butler
Journal:  Am J Med Genet       Date:  1990-03

7.  Increased hypothalamic neuropeptide Y expression following food deprivation.

Authors:  J D White; M Kershaw
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8.  The role of neuropeptide Y in the antiobesity action of the obese gene product.

Authors:  T W Stephens; M Basinski; P K Bristow; J M Bue-Valleskey; S G Burgett; L Craft; J Hale; J Hoffmann; H M Hsiung; A Kriauciunas
Journal:  Nature       Date:  1995-10-12       Impact factor: 49.962

9.  Weight-reducing effects of the plasma protein encoded by the obese gene.

Authors:  J L Halaas; K S Gajiwala; M Maffei; S L Cohen; B T Chait; D Rabinowitz; R L Lallone; S K Burley; J M Friedman
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Authors:  M G Carlson; W L Snead; A M Oeser; M G Butler
Journal:  J Lab Clin Med       Date:  1999-01

2.  Effects of MetAP2 inhibition on hyperphagia and body weight in Prader-Willi syndrome: A randomized, double-blind, placebo-controlled trial.

Authors:  Shawn E McCandless; Jack A Yanovski; Jennifer Miller; Cary Fu; Lynne M Bird; Parisa Salehi; Christine L Chan; Diane Stafford; M Jennifer Abuzzahab; David Viskochil; Sarah E Barlow; Moris Angulo; Susan E Myers; Barbara Y Whitman; Dennis Styne; Elizabeth Roof; Elisabeth M Dykens; Ann O Scheimann; Jaret Malloy; Dongliang Zhuang; Kristin Taylor; Thomas E Hughes; Dennis D Kim; Merlin G Butler
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3.  Plasma peptide YY and ghrelin levels in infants and children with Prader-Willi syndrome.

Authors:  Merlin G Butler; Douglas C Bittel; Zohreh Talebizadeh
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4.  Plasma obestatin and ghrelin levels in subjects with Prader-Willi syndrome.

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6.  Peptide YY, cholecystokinin, insulin and ghrelin response to meal did not change, but mean serum levels of insulin is reduced in children with Prader-Willi syndrome.

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7.  SnoRNA Snord116 (Pwcr1/MBII-85) deletion causes growth deficiency and hyperphagia in mice.

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Journal:  PLoS One       Date:  2008-03-05       Impact factor: 3.240

8.  Leptin replacement improves cognitive development.

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9.  Body composition, adipokines, bone mineral density and bone remodeling markers in relation to IGF-1 levels in adults with Prader-Willi syndrome.

Authors:  I Caroline van Nieuwpoort; Jos W R Twisk; Leopold M G Curfs; Paul Lips; Madeleine L Drent
Journal:  Int J Pediatr Endocrinol       Date:  2018-01-16

Review 10.  Hypothalamic neuropeptides and neurocircuitries in Prader Willi syndrome.

Authors:  Felipe Correa-da-Silva; Eric Fliers; Dick F Swaab; Chun-Xia Yi
Journal:  J Neuroendocrinol       Date:  2021-06-22       Impact factor: 3.627

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