Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency.
By I. S. Farooqi, G. Matarese, Graham M Lord, J. Keogh, E. Lawrence, Chizo Agwu, V. Sanna, S. Jebb, F. Perna, S. Fontana and 3 more. Journal of Clinical Investigation, 2002
1,548 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Epidemiology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/73c00396a0367a4951bfd6f796950a5274ebba1f
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In Endocrine and Autonomic Systems
In Epidemiology
In Nutrition and Dietetics
- Barry M. Popkin
- T. Lobstein
- S. O’Rahilly
- J. Berkley
- I. S. Farooqi
- Claire D. Bourke
- A. Prendergast
- A. Coll
Citations in the corpus
- The weight of leptin in immunity (2004, background): “Although the influence of thyroid and growth hormones on the effects of leptin remains elusive, it seems that leptin can affect thymic output and T-cell function independently of glucocorticoids, as congenitally leptin-deficient individuals have glucocorticoid levels within a normal range, but marke”
- Obesity and the role of adipose tissue in inflammation and metabolism. (2006, background): “There are certainly rare cases where mutations affecting the genes coding for either leptin or its receptor have been found in families with a high prevalence of morbid obesity (23–25), and leptin therapy does have a beneficial effect in children with congenital leptin deficiency (26, 27).”
- The Human Obesity Gene Map: The 2005 Update (2006, background): “11(19) Adra1b 5q23-q32 ADRA1B Adrenergic receptor, 1b Accelerated weight gain on high-fat diet (279) 19(50) Adra2a 10q24-q26 ADRA2A Transgene expresses adrenergic receptor 2 in adipose cells Transgene: aP2-driven human ADRA2A cDNA When expressed in Adra3bdeficient mice, leads to obesity.”
- Obesity in children and young people: a crisis in public health. (2004, background): “Three leptindeficient children have been treated with daily subcutaneous injections of recombinant human leptin for up to 4 years with sustained, beneficial effects on appetite, fat mass and hyperinsulinaemia (267).”
- Pediatric Obesity-Assessment, Treatment, and Prevention: An Endocrine Society Clinical Practice Guideline. (2017, positive): “…that reduce the production, secretion, or biological activity of leptin are associated with extreme hyperphagia, frequent infections, hypo-gonadotropic hypogonadism, and mild hypothyroidism; these features can be fully treated with subcutaneous injections of recombinant human leptin (105 – 107).”
- Recent advances in the relationship between obesity, inflammation, and insulin resistance. (2006, background): “Leptin-deficient mice or humans display an altered immune status [29-31].”
- Relationship of obesity with osteoporosis. (2007, background): “Treatment of children with congenital leptin deficiency with recombinant leptin leads to increased bone mass (31) and a sustained reduction in weight, predominantly as a result of a loss of fat (30,31).”
- The Hormonal Control of Food Intake (2007, positive): “It is life-saving in humans with congenital leptin deficiency (Farooqi et al., 2002), has dramatic effects on the metabolic state of patients with lipodystrophy (a metabolic disorder characterized by selective loss of body fat and low leptin levels) (Oral et al.”
- Metabolic Regulation of T Lymphocytes (2013, background): “Administration of recombinant leptin protein to leptin-deficient mice or humans reverses both the metabolic defects and immune abnormalities observed (148).”
- Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. (2015, background): “Leptin replacement facilitates pubertal development in ob/ob mice and leptin-deficient humans, establishing a crucial role of leptin in reproduction [54, 64, 65].”