Tracking of Leptin, Soluble Leptin Receptor, and the Free Leptin Index during Weight Loss and Regain in Children

Holm, Jens Christian; Gamborg, Michael; Ward, Leigh C.; Gammeltoft, Steen; Kaas-Ibsen, Karsten; Heitmann, Berit Lilienthal; Sørensen, Thorkild I A

doi:10.1159/000335121

Cited by 8 publications

(7 citation statements)

References 39 publications

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“…Мы применили этот расчетный показатель как маркер активности лептина у пациентов с МС. Наши данные о более высоком уровне свободных рецепторов леп-тина у лиц с нормальной массой тела по сравнению с пациентами с простым ожирением и МС, что соот-ветственно проявляется низким значением индекса свободного лептина, созвучны с результатами других исследователей [10,12,14,15,16].…”

Section: Discussionunclassified

“…Существует мнение, что индекс свободного лептина может быть лучшим маркером оценки лептинорези-стентности, чем лептин или растворимые рецепторы лептина [10,12,14,15]. Учитывая большой разброс данных системы лептина, гендерную и возрастную за-висимость, мы согласны с этой позицией.…”

Section: Discussionunclassified

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Leptin, soluble leptin receptor, and free leptin index in patients with metabolic syndrome

Смирнова¹,

Shulkina²

2017

Obes. metabol.

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Aim. To assess the levels of leptin, its soluble receptor, and index of the formation of free leptin in metabolic syndrome (MS). Materials and methods. The study included 110 individuals with obesity and overweight. The group 1 consisted of 70 patients with MS (IDF, 2005), the average body mass index (BMI) 38.4 4.4 kg/m2, aged 48.2 2.4 years, with arterial hypertension (AH) 12 degree, without regular antihypertensive therapy. Group 2 "healthy" obesity accounted for 40 patients aged 38.4 6.2 years, BMI 36.0 5.5 kg/m2 without hypertension and metabolic disorders. Group 3 consisted of 30 healthy persons, BMI 27.1 1.3 kg/m2. All patients were evaluated for insulin, HOMA index, leptin, leptin receptor, leptin free index (calculated as the ratio of leptin (ng/ml) to the leptin receptor (ng/ml), multiplied by 100). Results: In patients with MS as compared to other two groups there were higher levels of HOMA IR index, leptin and free leptin index. Values of leptin receptor in groups 1 and 2 did not differ significantly and were lower than in healthy persons. The free leptin index was significantly higher in MS group relative to the group 2 and 15 times higher than in the healthy individuals. Free leptin index correlated with values of BMI (R = 0.32; p = 0.02), blood pressure (R = 0.3; p = 0.04), uric acid (R = 0.27; p = 0.04), triglycerides (R = 0.42; p = 0.02), index HOMA-IR (R = 0.45; p = 0.02). Conclusions: Reduction of soluble leptin receptor, depending on the degree of abdominal obesity, may cause progression of leptin resistance in patients with MS. The levels of leptin and soluble leptin receptor appears to have dramatical gender differences. Calculation of free leptin index should be used for the objective evaluation of leptin resistance, regardless of gender, degree of obesity, and other metabolic parameters.

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Section: Discussionunclassified

Leptin, soluble leptin receptor, and free leptin index in patients with metabolic syndrome

Смирнова¹,

Shulkina²

2017

Obes. metabol.

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“…In lean individuals, leptin secretion from WAT increases after feeding to signal satiety and control energy balance by regulating glucose and fat metabolism. However, with adiposopathy, prolonged elevated leptin levels and reduced circulating soluble leptin receptors results in the development of a leptin-resistant state (Ogier et al, 2002;Holm et al, 2011). In addition to regulating satiety, leptin acts as an inflammatory cytokine to modulate the immune response, and the increased leptin levels with adiposopathy foster low-grade chronic inflammation (La Cava, 2017;Kumar et al, 2020).…”

Section: Changes In Endocrine Function Of Adipose Tissue In Obesitymentioning

confidence: 99%

Parental obesity-induced changes in developmental programming

Cechinel

Batabyal²,

Freishtat³

et al. 2022

Front. Cell Dev. Biol.

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Many studies support the link between parental obesity and the predisposition to develop adult-onset metabolic syndromes that include obesity, high blood pressure, dyslipidemia, insulin resistance, and diabetes in the offspring. As the prevalence of obesity increases in persons of childbearing age, so does metabolic syndrome in their descendants. Understanding how parental obesity alters metabolic programs in the progeny, predisposing them to adult-onset metabolic syndrome, is key to breaking this cycle. This review explores the basis for altered metabolism of offspring exposed to overnutrition by focusing on critical developmental processes influenced by parental obesity. We draw from human and animal model studies, highlighting the adaptations in metabolism that occur during normal pregnancy that become maladaptive with obesity. We describe essential phases of development impacted by parental obesity that contribute to long-term alterations in metabolism in the offspring. These encompass gamete formation, placentation, adipogenesis, pancreas development, and development of brain appetite control circuits. Parental obesity alters the developmental programming of these organs in part by inducing epigenetic changes with long-term consequences on metabolism. While exposure to parental obesity during any of these phases is sufficient to alter long-term metabolism, offspring often experience multiple exposures throughout their development. These insults accumulate to increase further the susceptibility of the offspring to the obesogenic environments of modern society.

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“…But in the case of obese individuals, leptin resistance develops decreased levels of circulating soluble leptin receptors (SLR). High leptin levels with low SLR make obese individuals resistant to leptin (22). Leptin receptors are present in the liver, skeletal muscles, pancreatic beta cells, and adipose tissue implicating its endocrine, autocrine, and paracrine roles in energy regulation.…”

Section: Leptinmentioning

confidence: 99%

Beslenme Faktörlerinin Obeziteye Bağlı Komplikasyonlar Üzerindeki Etkisi: Hipotiroidizm, Dislipidemi ve Hormonal Dengesizlik

AWASTHI¹,

BİGONİYA

Gupta

2022

Türk Diyab Obez / Turk J Diab Obes

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Obezite, dünya çapında yaygın olan en önemli yaşam tarzı bozukluklarından biridir. Artan obezite oranı, tiroid disfonksiyonu, dislipidemi, hormonal dengesizlik vb. hastalıkların ortaya çıkması ile ilişkilidir. Obezite, kalp hastalığı, ateroskleroz, insülin direnci, artrit, kas-iskelet sistemi bozuklukları ve kanser için risk faktörüdür. Bu makale, obezitenin dislipidemi, diyabet, hormonal dengesizlik ve hipotiroidizm ile ilişkisine dair içgörüler sunmaktadır. Leptin, insülin, seks hormonları ve büyüme hormonları iştahı, metabolizmayı ve vücut yağ dağılımını etkilediğinden hormonların aşırı veya yetersiz salınımı obeziteye yol açabilir. Makale, metabolik düzensizliğin obezite ile ilişkisi ve ilgili hastalıkların daha da geliştirilmesi hakkında bir inceleme sunmaktadır. Bu makale aynı zamanda diyet liflerinin ve balık proteininin metabolik değişiklikler, hormonal dengesizlik ve obezite ile ilişkili hiperlipidemi üzerindeki etkilerini de özetlemektedir. Bu makale, obezite ile ilgili bozuklukları yönetmek için yararlı olan lif ve diyet protein tüketimi gibi diyet müdahalesinin rolünü detaylandırdı. Potansiyel nutrasötik ürünler sık besin kaynakları olarak tüketilmektedir. Yine de, kaliteli insan klinik deney verileri eksiktir, bu da nutrasötiklerin güvenliğini ve etkinliğini değerlendirmek için önemli bilimsel çalışmalara ihtiyaç olduğunu gösterir.

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Tracking of Leptin, Soluble Leptin Receptor, and the Free Leptin Index during Weight Loss and Regain in Children

Cited by 8 publications

References 39 publications

Leptin, soluble leptin receptor, and free leptin index in patients with metabolic syndrome

Leptin, soluble leptin receptor, and free leptin index in patients with metabolic syndrome

Parental obesity-induced changes in developmental programming

Beslenme Faktörlerinin Obeziteye Bağlı Komplikasyonlar Üzerindeki Etkisi: Hipotiroidizm, Dislipidemi ve Hormonal Dengesizlik

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