Abundance of Circulating Preadipocyte Factor 1 in Early Life

Zegher, Francis de; Díaz, Marta; Sebastiani, Giorgia; Martı́n-Ancel, Ana; Sánchez‐Infantes, David; López‐Bermejo, Abel; Ibáñez, Lourdes

doi:10.2337/dc11-1990

Cited by 30 publications

(25 citation statements)

References 12 publications

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“…Altogether time-related decrease in DLK1 expression level seems to be a mandatory step for normal myogenesis (White et al, 2008). In support to our findings in skeletal muscle of intrauterine growthrestricted fetuses, it has been shown that circulating levels of soluble DLK1 are higher in small-for-gestational age babies at birth (de Zegher et al, 2012). In the present study, NCAM1/CD56, a gene encoding a cell surface marker in precursor cells carrying a high myogenic potential (Perruchot et al, 2013), also tended to be higher in the lightest fetuses.…”

Section: Discussionsupporting

confidence: 80%

Delayed muscle development in small pig fetuses around birth cannot be rectified by maternal early feed restriction and subsequent overfeeding during gestation

Perruchot

Lefaucheur

Louveau

et al. 2015

Animal

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Intrauterine variations in nutrient allowance can alter body composition and tissue features of the porcine offspring around birth. This study aimed to determine the effects of fetal weight variations between littermates and of maternal dietary regimen during gestation on fetal muscle traits just before birth. Fourteen pregnant gilts were reared under a conventional (control, CTL; n = 7) or an experimental (treatment, TRT; n = 7) dietary regimen during gestation. The dietary treatment provided 70% of the protein and digestible energy contents of the CTL diet during the first 70 days of gestation and then, 115% of the protein and digestible energy contents up to farrowing. At 110 days of gestation, sows were sacrificed and one fetus having a low (824 ± 140 g) and one having a normal (1218 ± 192 g) BW per litter were sampled. Irrespective of maternal dietary regimen, the longissimus muscle of the small fetuses exhibited higher expression levels of DLK1/Pref1 and NCAM1/CD56, two genes known to be downregulated during normal skeletal muscle development. Expression levels of the embryonic isoform of the myosin heavy chain (MyHC), both at the mRNA and at the protein levels, were also higher in small fetuses. In addition, the ratios of perinatal to embryonic and of adult fast to developmental MyHC isoforms were generally lower in light fetuses compared with their medium-weight littermates. These modifications suggest a delayed myofiber development in spontaneous growth-retarded fetuses. Finally, GLUT1 was expressed to a lesser extent in the muscle of small v. normal fetuses, suggesting decreased ability for glucose uptake in muscle. Initial feed restriction and subsequent overfeeding of sows during gestation led to a lower expression of the myogenic factor MYOD1, a prerequisite for myogenic initiation in skeletal muscle. This maternal strategy was also associated with a lower expression level of insulin-like growth factor 1 receptor (IGFR) but an upregulation of IGF2. This suggests an altered susceptibility of muscle cells to IGFs' signal in fetuses from treated sows. Altogether, intrauterine growth restriction impaired fetal muscle development, and restricted feeding followed by overfeeding of gestating sows did not allow small fetuses to recover normal contractile and metabolic characteristics.

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Section: Discussionsupporting

confidence: 80%

Delayed muscle development in small pig fetuses around birth cannot be rectified by maternal early feed restriction and subsequent overfeeding during gestation

Perruchot

Lefaucheur

Louveau

et al. 2015

Animal

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“…Recent studies suggest that individuals born SGA display significant alterations to their SAT functions, of which impaired expandability and capacity to store excess fat represent core metabolic changes [33,34]. It is likely that the finding of increased lipolysis in SGA individuals after an 8 h overnight fast may be a metabolic manifestation of their impaired capability to accumulate fat, and that "excess fat" is therefore released at an increased rate after an overnight fast.…”

Section: Discussionmentioning

confidence: 99%

Metabolic response to 36 hours of fasting in young men born small vs appropriate for gestational age

Jørgensen

Brøns²,

Bluck³

et al. 2014

Diabetologia

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Aims/hypothesis Being born small for gestational age (SGA) is associated with an increased risk of type 2 diabetes in an affluent society, but could confer an improved chance of survival during sparse living conditions. We studied whether insulin action and other metabolic responses to prolonged fasting differed between 21 young adults born SGA and 18 matched controls born appropriate for gestational age (AGA). Methods A frequently sampled IVGTT and indirect calorimetry measurements were performed after a 36 h fast. Endogenous glucose production, insulin sensitivity (S I ), first-phase insulin secretion and glucose effectiveness were estimated by stable isotope tracer techniques and minimal modelling. Muscle and fat biopsies were obtained after 35 h of fasting. Results During fasting, SGA individuals experienced a more pronounced decrease in serum insulin and lower plasma triacylglycerol levels compared with AGA individuals. In addition, energy expenditure decreased in SGA but increased in AGA individuals. After fasting, SGA individuals displayed lower fat oxidation than AGA individuals. S G was reduced in SGA compared with AGA individuals, whereas hepatic or whole body insulin action (S I ) did not differ between groups. SGA individuals had increased muscle PPARGC1A DNA methylation. We found no differences in adipose tissue PPARGC1A DNA methylation, muscle and adipose tissue PPARGC1A mRNA expression, or muscle glycogen levels between the groups. Conclusion Compared with AGA individuals, SGA individuals displayed a more energy-conserving and energy-conserving cardiometabolic response to 36 h fasting. The role of increased muscle PPARGC1A DNA methylation in mediating this response requires further study.

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“…Young, healthy men born with a low birthweight have significant changes in body fat content and distribution, increased rate of lipolysis and impaired preadipocyte maturation (35,36), which may contribute to the development of whole-body as well as adipose tissue and hepatic insulin resistance later in life. De Zegher et al found that fetal growth restriction was associated with increased circulating levels of preadipocyte factor 1 (Pref-1), which inhibits adipocyte differentiation (37). These data suggest that Pref-1 may be a mediator of reduced adipocyte differentiation in growth-restrained fetuses, and thus of a reduction in life-long lipid storage capacity and thereby of adult vulnerability to metabolic disease, once lipid storage becomes an issue.…”

Section: Adipose Tissue Expandabilitymentioning

confidence: 95%

MECHANISMS IN ENDOCRINOLOGY: Skeletal muscle lipotoxicity in insulin resistance and type 2 diabetes: a causal mechanism or an innocent bystander?

Brøns

Grunnet

2017

European Journal of Endocrinology

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Dysfunctional adipose tissue is associated with an increased risk of developing type 2 diabetes (T2D). One characteristic of a dysfunctional adipose tissue is the reduced expandability of the subcutaneous adipose tissue leading to ectopic storage of fat in organs and/or tissues involved in the pathogenesis of T2D that can cause lipotoxicity. Accumulation of lipids in the skeletal muscle is associated with insulin resistance, but the majority of previous studies do not prove any causality. Most studies agree that it is not the intramuscular lipids per se that causes insulin resistance, but rather lipid intermediates such as diacylglycerols, fatty acyl-CoAs and ceramides and that it is the localization, composition and turnover of these intermediates that play an important role in the development of insulin resistance and T2D. Adipose tissue is a more active tissue than previously thought, and future research should thus aim at examining the exact role of lipid composition, cellular localization and the dynamics of lipid turnover on the development of insulin resistance. In addition, ectopic storage of fat has differential impact on various organs in different phenotypes at risk of developing T2D; thus, understanding how adipogenesis is regulated, the interference with metabolic outcomes and what determines the capacity of adipose tissue expandability in distinct population groups is necessary. This study is a review of the current literature on the adipose tissue expandability hypothesis and how the following ectopic lipid accumulation as a consequence of a limited adipose tissue expandability may be associated with insulin resistance in muscle and liver.Correspondence should be addressed to C Brøns Email charlotte.broens@regionh.dk Invited Author's profile Charlotte Brøns PhD, is currently head of the Department of Diabetes and Metabolism at Rigshospitalet, and adjunct Associate Professor at the University of Copenhagen, Denmark. Her scientific expertise lies within the field of metabolism and integrative physiology with an extensive focus on the physiologic and molecular mechanisms underlying the etiology and pathophysiology of type 2 diabetes primarily in individuals exposed to intrauterine over-(gestational diabetes) and under-nutrition (low birth weight).

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Abundance of Circulating Preadipocyte Factor 1 in Early Life

Cited by 30 publications

References 12 publications

Delayed muscle development in small pig fetuses around birth cannot be rectified by maternal early feed restriction and subsequent overfeeding during gestation

Delayed muscle development in small pig fetuses around birth cannot be rectified by maternal early feed restriction and subsequent overfeeding during gestation

Metabolic response to 36 hours of fasting in young men born small vs appropriate for gestational age

MECHANISMS IN ENDOCRINOLOGY: Skeletal muscle lipotoxicity in insulin resistance and type 2 diabetes: a causal mechanism or an innocent bystander?

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