MicroRNAs in the growth plate are responsive to nutritional cues: association between miR-140 and SIRT1

Pando, Rakefet; Even-Zohar, Naomi; Shtaif, Biana; Edry, Liat; Shomron, Noam; Phillip, Moshe; Gat-Yablonski, Galia

doi:10.1016/j.jnutbio.2011.09.010

Cited by 42 publications

(52 citation statements)

References 55 publications

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“…IGF1 serves as both the main mediator of GH action and as a GHindependent growth factor, and is a well-known growth factor for both chondrocytes and osteoblasts. IGF1 concentrations are responsive to changing nutritional status and intake of amino acids and free fatty acids (Mosier & Jansons 1976, Hermanussen et al 1996, and serum IGF1 levels were reduced by RES in all animals studied (Lowe et al 1989, Devlin et al 2010, Pando et al 2012). The reduced serum IGF1 level is likely to contribute to the cortical thinning observed, as a similar phenotype was also observed in liver-specific IGF1 deficient lid/lid mice (Yakar et al 2002).…”

Section: Discussionmentioning

confidence: 92%

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Pando

Masarwi

Shtaif

et al. 2014

Journal of Endocrinology

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Growth stunting constitutes the most common effect of malnutrition. When the primary cause of malnutrition is resolved, catch-up (CU) growth usually occurs. In this study, we have explored the effect of food restriction (RES) and refeeding on bone structure and mechanical properties. Sprague-Dawley male rats aged 24 days were subjected to 10 days of 40% RES, followed by refeeding for 1 (CU) or 26 days long-term CU (LTCU). The rats fed ad libitum served as controls. The growth plates were measured, osteoclasts were identified using tartrate-resistant acid phosphatase staining, and micro-computed tomography (CT) scanning and mechanical testing were used to study structure and mechanical properties. Micro-CT analysis showed that RES led to a significant reduction in trabecular BV/TV and trabecular number (Tb.N), concomitant with an increase in trabecular separation (Tb.Sp). Trabecular BV/TV and Tb.N were significantly greater in the CU group than in the RES in both short-and long-term experiments. Mechanical testing showed that RES led to weaker and less compliant bones; interestingly, bones of the CU group were also more fragile after 1 day of CU. Longer term of refeeding enabled correction of the bone parameters; however, LTCU did not achieve full recovery. These results suggest that RES in young rats attenuated growth and reduced trabecular bone parameters. While nutrition-induced CU growth led to an immediate increase in epiphyseal growth plate height and active bone modeling, it was also associated with a transient reduction in bone quality. This should be taken into consideration when treating children undergoing CU growth.

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Section: Discussionmentioning

confidence: 92%

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Pando

Masarwi

Shtaif

et al. 2014

Journal of Endocrinology

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“…Elevated levels of circulating pro-inflammatory cytokines can reduce energy uptake and metabolism as well as induce protein catabolism. Studies in mice have shown a significant decrease in IGF1 levels as well as a reduction in GH receptor expression in the growth plate during food restriction (Gat-Yablonski et al 2008, Pando et al 2012. Furthermore, malnutrition often leads to delayed sexual development that indirectly results in growth retardation linked with negative effects on the GH/IGF1 axis (Ezri et al 2012).…”

Section: Impact Of Inflammation On Bone Growthmentioning

confidence: 99%

RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth

Sederquist¹,

Fernandez-Vojvodich²,

Zaman³

et al. 2014

Journal of Molecular Endocrinology

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Children with inflammatory diseases usually display abnormal growth patterns as well as delayed puberty. This is a result of several factors related to the disease itself, such as malnutrition, hypercortisolism, and elevated levels of pro-inflammatory cytokines. These factors in combination with glucocorticoid treatment contribute to growth retardation during chronic inflammation by systemically affecting the major regulator of growth, the GH/IGF1 axis. However, recent studies have also shown evidence of a direct effect of these factors at the growth plate level. In conditions of chronic inflammation, pro-inflammatory cytokines are upregulated and released into the circulation. The most abundant of these, tumor necrosis factor a, interleukin 1b (IL1b), and IL6, are all known to directly act on growth plate cartilage to induce apoptosis and thereby suppress bone growth. Both clinical and experimental studies have shown that growth retardation can partly be rescued when these cytokines are blocked. Therefore, therapy modulating the local actions of these cytokines may be effective for preventing growth failure in patients with chronic inflammatory disorders. In this review, we report the current knowledge of inflammatory cytokines and their role in regulating bone growth.

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“…Our group (G.G.-Y.) observed a marked reduction of GH receptor (GHR) and IGF-1R in the GP of food-restricted animals [47, 48], indicating that the GP is rendered GH- and IGF-1-resistant at the receptor level during food restriction [47]. Interestingly, levels of IGF-1 and IGF-1R expression increased already after one day of re-feeding [47, 48], enabling CU growth.…”

Section: Systemic Factors In Malnutrition and Cu Growthmentioning

confidence: 99%

Effect of Nutrition on Statural Growth

Gat-Yablonski

Luca

2017

Horm Res Paediatr

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In children, proper growth and development are often regarded as a surrogate marker for good health. A complex system controls the initiation, rate, and cessation of growth, and thus gives a wonderful example of the interactions between genetics, epigenetics, and environmental factors (especially stress and nutrition). Malnutrition is considered a leading cause of growth attenuation in children. This review summarizes our current knowledge regarding the mechanisms linking nutrition and skeletal growth, including systemic factors, such as insulin, growth hormone, insulin-like growth factor-1, fibroblast growth factor-21, etc., and local mechanisms, including mTOR, miRNAs, and epigenetics. Studying the molecular mechanisms regulating skeletal growth may lead to the establishment of better nutritional and therapeutic regimens for more effective linear growth in children with malnutrition and growth abnormalities.

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MicroRNAs in the growth plate are responsive to nutritional cues: association between miR-140 and SIRT1

Cited by 42 publications

References 55 publications

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

Bone quality is affected by food restriction and by nutrition-induced catch-up growth

RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth

Effect of Nutrition on Statural Growth

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