Metabolism - Clinical and Experimental
Volume 44, Issue 8 , Pages 1033-1037, August 1995

Is obesity-related insulin status the cause of blunted growth hormone secretion in turner's syndrome?

  • Fabrizio Vaccaro

      Affiliations

    • Department of Pediatrics, “Tor Vergata” University, Rome, Italy
    • Department of Pediatrics, “La Sapienza” University, Rome, Italy
  • ,
  • Stefano Cianfarani

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Stefano Cianfarani, MD, Department of Pediatrics, Dip.San.Pubbl.Biol.Cell., “Tor Vergata” University, via di Tor Vergata, 135, 00133-Rome, Italy.
    • Department of Pediatrics, “Tor Vergata” University, Rome, Italy
    • Department of Pediatrics, “La Sapienza” University, Rome, Italy
  • ,
  • Anna Maria Pasquino

      Affiliations

    • Department of Pediatrics, “Tor Vergata” University, Rome, Italy
    • Department of Pediatrics, “La Sapienza” University, Rome, Italy
  • ,
  • Brunetto Boscherini

      Affiliations

    • Department of Pediatrics, “Tor Vergata” University, Rome, Italy
    • Department of Pediatrics, “La Sapienza” University, Rome, Italy

Received 18 July 1994; accepted 29 November 1994.

Abstract 

Growth hormone (GH) secretion is reduced in girls with Turner's syndrome (TS) at pubertal age. We have recently proposed that the impairment of GH release in TS girls might be secondary to obesity. In the present study, we assessed the influence of overweight-related insulin status on spontaneous GH secretion in a group of 15 TS girls. Eighteen age-matched short normal subjects and six short obese prepubertal children were chosen as controls. Anthropometry, spontaneous GH secretion, insulin-like growth factor-I (IGF-I) serum levels, basal fasting insulin, and glucose concentrations were determined. The percentage of ideal body weight (IBW) was used as an index of nutritional status. Baseline fasting glucose (milligrams per deciliter) to insulin (milliunits per liter) ratio (G/I) was chosen as an index of insulin resistance. GH secretion was significantly lower in TS girls than in non-obese children (P < .005), whereas no significant difference was seen between TS and obese subjects. IGF-I levels were not statistically different in all groups. GH secretion was confirmed to be related to the degree of overweight (r = −.52, P < .05 in TS girls and r = −.74, P < .0001 in control group). G/I was closely related to both the percentage of IBW (r = −.59, P = .02) and GH level (r = .57, P = .03) in TS patients. These results confirm that the blunted GH secretion in TS patients is dependent on nutritional status, and suggest that insulin resistance secondary to overweight might represent the pathophysiologic link between the obesity-related metabolic status and impaired GH secretion.

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PII: 0026-0495(95)90101-9

Metabolism - Clinical and Experimental
Volume 44, Issue 8 , Pages 1033-1037, August 1995