Insulin resistance depends on GH counter-regulation in two syndromes of short stature

Guevara‐Aguirre, Jaime; Guevara, Alexandra; Bahamonde, Marisol

doi:10.1016/j.ghir.2017.12.012

Cited by 9 publications

(4 citation statements)

References 23 publications

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“…Reasons for this include the following: (i) the growth hormone receptor gene is closely related to the occurrence of short stature. Previous studies have shown that the growth hormone receptor gene mutation will affect the growth hormone and the receptor binding, and then cause signaling disorders, affect the function of growth hormone, and impede growth and development [ 15 ]. (ii) Adolescent developmental delay, which means that no secondary sexual characteristics appear at the age of 13 in girls or 14 in boys, may affect height development to some extent [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Analysis of Prevalence, Influencing Factors, and Countermeasures of Short Stature in Children and Adolescents Aged 6∼14 in Furong District, Changsha City, in 2020

Chen

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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In recent years, children’s and adolescents’ growth and development issues have received increasing attention with the socioeconomic development. The etiology of child short stature involves heredity, race, sex, nutrition, and a variety of endocrine hormones, which is very complex. The age of 6∼14 is the key period of children’s development. Understanding the height characteristics, the prevalence of short stature, and its influencing factors at this stage and formulating preventive measures as soon as possible are conducive to improving the average height of children and reducing the incidence of short stature. In this study, cluster sampling was used to select 56,865 children and adolescents aged 6∼14 years old from 40 primary and secondary schools in Furong District of Changsha City, and the height of each child and adolescent was measured. The results showed that the overall crude prevalence of short stature in children aged 6∼14 in Furong District of Changsha is 2.82%. Growth hormone level <10 μg/L, pubertal retardation, familial short stature, low egg intake, and intrauterine growth retardation are independent risk factors affecting the occurrence of short stature. In order to improve the status quo of short stature of children aged 6∼14 in Furong District, Changsha City, targeted intervention should be strengthened for people with combined high risk factors.

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Section: Discussionmentioning

confidence: 99%

Analysis of Prevalence, Influencing Factors, and Countermeasures of Short Stature in Children and Adolescents Aged 6∼14 in Furong District, Changsha City, in 2020

Chen

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Reduced hepatic glucose production/gluconeogenesis was discussed as a potential cause for juvenile hypoglycemia in LS patients (10,69).…”

Section: Altered Endogenous Glucose Productionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Transient juvenile hypoglycemia in growth hormone receptor deficiency – mechanistic insights from Laron syndrome and tailored animal models

Hinrichs

Bidlingmaier

Kopchick

et al. 2021

European Journal of Endocrinology

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Aim of the study is to find possible explanations for vanishing juvenile hypoglycemia in growth hormone receptor deficiency (GHRD) in human patients and animal models. We reviewed parameters of glucose metabolism in distinct age groups in two human cohorts (Israeli and Ecuadorian) of Laron syndrome (LS) patients, a mouse model (Ghr-KO mouse) and provide additional data for a porcine model (GHR-KO pig). Juvenile hypoglycemia is a common symptom of GHRD and vanishes in adulthood. In the Israeli cohort, developing metabolic syndrome is associated with decreasing insulin sensitivity, insulinopenia and glucose intolerance, increasing glucose levels with age. In Ecuadorian patients and both animal models, insulin sensitivity is preserved or even enhanced. Alterations in food intake and energy consumption do not explain the differences in glucose levels, neither is the accumulation of body fat associated with negative effects in the Ecuadorian cohort or the animal models. A reduced beta cell mass and resulting insulin secretory capacity is common and leads to glucose intolerance in Ghr-KO mice, while glucose tolerance is preserved in Ecuadorian patients and the GHR-KO pig. In human patients and the GHR-KO pig, a simultaneous occurrence of normoglycemia with the onset of puberty is reported. Reduced gluconeogenesis in GHRD is discussed to cause the juvenile hypoglycemia and a counter regulatory stimulation of gluconeogenesis can be hypothesized. A coherent study assessing endogenous glucose production and beta-cell capacity in the hypoglycemic and normoglycemic age group is needed. This can be performed in GHR-KO pigs, including castrated animals.

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“…Milk consumption and increased IGF-1 serum levels are associated with increased linear growth and body mass index [73,74]. Remarkably, untreated individuals with Laron syndrome due to defective GH receptor signaling and congenital IGF-1 deficiency have less IR and lower incidence of T2D than their relatives [75][76][77]. In fact, an association of free IGF-1 serum levels and T2D has been reported in the Nurses' Health Study [78], whereas a nested case-cohort study within the EPIC-Potsdam Study found no association between total IGF-1 serum concentrations with risk of T2D [79].…”

Section: Insulin-like Growth Factormentioning

confidence: 99%

The impact of persistent milk consumption in the pathogenesis of type 2 diabetes mellitus

Melnik¹

2019

FFHD

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Background: Milk and sugar are excessively consumed in a Western diet. There is increasing epidemiological evidence that the intake of unfermented pasteurized cow´s milk is associated with an increased risk of type 2 diabetes mellitus (T2D). It is the intention of this review to provide translational biochemical evidence for milk´s diabetogenic mode of action. Milk proteins provide the highest amounts of branched-chain amino acids (BCAAs) and thus contribute to total BCAA intake, which enhances BCAA plasma levels associated with increased risk of T2D. The consumption of pasteurized milk raises plasma levels of miRNA-29b, which is a diabetogenic miRNA promoting insulin resistance (IR). miRNA29b inhibits the activity of branched-chain-keta acid dehydrogenase, the rate limiting enzyme of BCAA catabolism, which is impaired in patients with IR and T2D. Milk consumption stimulates mTORC1 activity and increases insulin synthesis. -cell mTORC1 is overactivated in T2D patients resulting in impaired autophagy which enhances endoplasmic reticulum (ER) stress associated with a greater risk of early -cell apoptosis, the pathogenic hallmark of T2D. Chronic insulinotropic action of milk-derived BCAAs, IR-promoting mTORC1 overactivity, and miRNA-29b signaling combined with excessive glucose-mediated insulin secretion overburden -cell insulin homeostasis. Epidemiological and translational evidence identifies continued milk intake as a promoter of T2D, the most common metabolic disease of Western civilization. Keywords: Branched-chain amino acids, branched-chain-keto acid dehydrogenase, diabetes mellitus type 2, insulin resistance, milk, miRNA-29b, mechanistic target of rapamycin complex 1.

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Insulin resistance depends on GH counter-regulation in two syndromes of short stature

Cited by 9 publications

References 23 publications

Analysis of Prevalence, Influencing Factors, and Countermeasures of Short Stature in Children and Adolescents Aged 6∼14 in Furong District, Changsha City, in 2020

Analysis of Prevalence, Influencing Factors, and Countermeasures of Short Stature in Children and Adolescents Aged 6∼14 in Furong District, Changsha City, in 2020

MECHANISMS IN ENDOCRINOLOGY: Transient juvenile hypoglycemia in growth hormone receptor deficiency – mechanistic insights from Laron syndrome and tailored animal models

The impact of persistent milk consumption in the pathogenesis of type 2 diabetes mellitus

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