Increased OB gene expression leads to elevated plasma leptin concentrations in patients with chronic primary hyperinsulinemia

Monica D'Adamo, Angela Buongiorno, Ettore Maroccia, Frida Leonetti, Fabrizio Barbetti, Andrea Giaccari, Domenico Zorretta, Guido Tamburrano, Paolo Sbraccia

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Leptin, a hormone secreted by adipocytes, decreases food intake and increases energy expenditure. The role of insulin in the regulation of leptin secretion is poorly understood and is still a topic of debate. Insulin increases leptin mRNA synthesis in rodents, but in humans, the available data are discordant. To investigate the role of chronic hyperinsulinemia in the regulation of plasma leptin concentrations, we studied 13 patients with surgically confirmed insulinoma before and after tumor removal, along with 15 healthy control subjects matched for sex, age, and BMI. Immunoreactive plasma leptin levels were measured by radioimmunoassay; leptin mRNA levels were also determined by reverse transcription-competitive polymerase chain reaction in a subgroup of six patients with insulinoma and six control subjects. All determinations were made with subjects in the fasting state. Plasma leptin concentrations correlated positively with leptin mRNA levels (r = 0.880, P <0.001). Leptin levels, both plasma protein and mRNA, were significantly higher in the insulinoma patients than in the control subjects (plasma protein: 17.5 ± 3.6 vs. 2.9 ± 0.4 ng/ml, respectively, P <0.001; mRNA: 0.98 ± 0.33 vs. 0.19 ± 0.064 amol/μg RNA, respectively, P <0.05), and they correlated positively with fasting plasma insulin levels in the patients with insulinoma (plasma protein: r = 0.686, P <0.01; mRNA: 0.796, P <0.05). Finally, removal of the insulin-secreting tumor was followed by the normalization of plasma leptin levels. In summary, in patients with insulinoma, 1) plasma leptin levels and leptin mRNA are elevated; 2) a direct relationship exists between leptin, both circulating protein and mRNA, and insulin concentrations; and 3) plasma leptin returns to normal levels after tumor removal. These data, therefore, support a role for insulin in the chronic regulation of leptin gene expression.

Original languageEnglish
Pages (from-to)1625-1629
Number of pages5
JournalDiabetes
Volume47
Issue number10
DOIs
Publication statusPublished - 1998

Fingerprint

Hyperinsulinism
Leptin
Gene Expression
Insulinoma
Messenger RNA
Insulin
Blood Proteins
Fasting
Neoplasms
Gene Expression Regulation
Adipocytes
Energy Metabolism
Reverse Transcription
Radioimmunoassay
Rodentia
Healthy Volunteers

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Increased OB gene expression leads to elevated plasma leptin concentrations in patients with chronic primary hyperinsulinemia. / D'Adamo, Monica; Buongiorno, Angela; Maroccia, Ettore; Leonetti, Frida; Barbetti, Fabrizio; Giaccari, Andrea; Zorretta, Domenico; Tamburrano, Guido; Sbraccia, Paolo.

In: Diabetes, Vol. 47, No. 10, 1998, p. 1625-1629.

Research output: Contribution to journalArticle

D'Adamo, M, Buongiorno, A, Maroccia, E, Leonetti, F, Barbetti, F, Giaccari, A, Zorretta, D, Tamburrano, G & Sbraccia, P 1998, 'Increased OB gene expression leads to elevated plasma leptin concentrations in patients with chronic primary hyperinsulinemia', Diabetes, vol. 47, no. 10, pp. 1625-1629. https://doi.org/10.2337/diabetes.47.10.1625
D'Adamo, Monica ; Buongiorno, Angela ; Maroccia, Ettore ; Leonetti, Frida ; Barbetti, Fabrizio ; Giaccari, Andrea ; Zorretta, Domenico ; Tamburrano, Guido ; Sbraccia, Paolo. / Increased OB gene expression leads to elevated plasma leptin concentrations in patients with chronic primary hyperinsulinemia. In: Diabetes. 1998 ; Vol. 47, No. 10. pp. 1625-1629.
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AU - D'Adamo, Monica

AU - Buongiorno, Angela

AU - Maroccia, Ettore

AU - Leonetti, Frida

AU - Barbetti, Fabrizio

AU - Giaccari, Andrea

AU - Zorretta, Domenico

AU - Tamburrano, Guido

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N2 - Leptin, a hormone secreted by adipocytes, decreases food intake and increases energy expenditure. The role of insulin in the regulation of leptin secretion is poorly understood and is still a topic of debate. Insulin increases leptin mRNA synthesis in rodents, but in humans, the available data are discordant. To investigate the role of chronic hyperinsulinemia in the regulation of plasma leptin concentrations, we studied 13 patients with surgically confirmed insulinoma before and after tumor removal, along with 15 healthy control subjects matched for sex, age, and BMI. Immunoreactive plasma leptin levels were measured by radioimmunoassay; leptin mRNA levels were also determined by reverse transcription-competitive polymerase chain reaction in a subgroup of six patients with insulinoma and six control subjects. All determinations were made with subjects in the fasting state. Plasma leptin concentrations correlated positively with leptin mRNA levels (r = 0.880, P <0.001). Leptin levels, both plasma protein and mRNA, were significantly higher in the insulinoma patients than in the control subjects (plasma protein: 17.5 ± 3.6 vs. 2.9 ± 0.4 ng/ml, respectively, P <0.001; mRNA: 0.98 ± 0.33 vs. 0.19 ± 0.064 amol/μg RNA, respectively, P <0.05), and they correlated positively with fasting plasma insulin levels in the patients with insulinoma (plasma protein: r = 0.686, P <0.01; mRNA: 0.796, P <0.05). Finally, removal of the insulin-secreting tumor was followed by the normalization of plasma leptin levels. In summary, in patients with insulinoma, 1) plasma leptin levels and leptin mRNA are elevated; 2) a direct relationship exists between leptin, both circulating protein and mRNA, and insulin concentrations; and 3) plasma leptin returns to normal levels after tumor removal. These data, therefore, support a role for insulin in the chronic regulation of leptin gene expression.

AB - Leptin, a hormone secreted by adipocytes, decreases food intake and increases energy expenditure. The role of insulin in the regulation of leptin secretion is poorly understood and is still a topic of debate. Insulin increases leptin mRNA synthesis in rodents, but in humans, the available data are discordant. To investigate the role of chronic hyperinsulinemia in the regulation of plasma leptin concentrations, we studied 13 patients with surgically confirmed insulinoma before and after tumor removal, along with 15 healthy control subjects matched for sex, age, and BMI. Immunoreactive plasma leptin levels were measured by radioimmunoassay; leptin mRNA levels were also determined by reverse transcription-competitive polymerase chain reaction in a subgroup of six patients with insulinoma and six control subjects. All determinations were made with subjects in the fasting state. Plasma leptin concentrations correlated positively with leptin mRNA levels (r = 0.880, P <0.001). Leptin levels, both plasma protein and mRNA, were significantly higher in the insulinoma patients than in the control subjects (plasma protein: 17.5 ± 3.6 vs. 2.9 ± 0.4 ng/ml, respectively, P <0.001; mRNA: 0.98 ± 0.33 vs. 0.19 ± 0.064 amol/μg RNA, respectively, P <0.05), and they correlated positively with fasting plasma insulin levels in the patients with insulinoma (plasma protein: r = 0.686, P <0.01; mRNA: 0.796, P <0.05). Finally, removal of the insulin-secreting tumor was followed by the normalization of plasma leptin levels. In summary, in patients with insulinoma, 1) plasma leptin levels and leptin mRNA are elevated; 2) a direct relationship exists between leptin, both circulating protein and mRNA, and insulin concentrations; and 3) plasma leptin returns to normal levels after tumor removal. These data, therefore, support a role for insulin in the chronic regulation of leptin gene expression.

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