Long-term type 1 diabetes impairs decidualization and extracellular matrix remodeling during early embryonic development in mice

Favaro, Rodolfo R.; Salgado, Renato M.; Covarrubias, Ambart E.; Bruni, Fernanda Miriane; Lima, Carla; Fortes, Zuleica Bruno; Zorn, Telma Maria Tenório

doi:10.1016/j.placenta.2013.09.012

Cited by 26 publications

(24 citation statements)

References 39 publications

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“…Favaro et al studied extracellular matrix remodeling in a mouse model of pregnancy complicated by longstanding type 1 diabetes characterized by high glucose levels, and they found a significantly increased deposition of type I collagen in the decidua. 18 Our findings in human placenta are in line with their results obtained in the animal model. It is likely that we only found a low fold increase in the abundance of collagen alpha-1 XIV chain because the GDM women under study were well controlled, and the pathological condition was present only in a limited time window.…”

Section: Resultssupporting

confidence: 90%

“…A slightly higher abundance of collagen alpha‐1 chain in GDM placentas was found. Favaro et al studied extracellular matrix remodeling in a mouse model of pregnancy complicated by longstanding type 1 diabetes characterized by high glucose levels, and they found a significantly increased deposition of type I collagen in the decidua . Our findings in human placenta are in line with their results obtained in the animal model.…”

Section: Resultssupporting

confidence: 90%

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Is the placental proteome impaired in well‐controlled gestational diabetes?

et al. 2019

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In pregnancy complicated by gestational diabetes mellitus (GDM), the human placenta shows several pathological functional and structural changes, but the extent to which maternal glycemic control contributes to placental abnormalities remains unclear. The aim of this study was to profile and compare the proteome of placentas from healthy pregnant women and those with GDM, to investigate the placenta‐specific protein composition and possible changes of its function in presence of GDM. Quantitative proteomic analysis, based on LC‐MSE approach, revealed that higher (approximately 15% increase) levels of galectin 1 and collagen alpha‐1 XIV chain (although the difference regarding the latter was at the limit of significance) were present in GDM samples, while heat shock 70 kDa protein 1A/1B was less abundant in GDM placental tissue. These data seem to indicate that GDM, when well controlled, did not markedly affect the placental proteome.

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Section: Resultssupporting

confidence: 90%

Section: Resultssupporting

confidence: 90%

Is the placental proteome impaired in well‐controlled gestational diabetes?

et al. 2019

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“…Interestingly, lumican has also been observed in the decidua of diabetic patients (60,61). Further investigations of these 348 and other candidates may uncover new skeletal regulators of energy metabolism.…”

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confidence: 91%

PHOSPHO1, a novel skeletal regulator of insulin resistance and obesity

Suchacki

Morton

Vary

et al. 2020

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26The skeleton is recognised as a key endocrine regulator of metabolism. Here we show that mice lacking the bone 27 mineralization enzyme PHOSPHO1 (Phospho1 -/-) exhibited improved basal glucose homeostasis and resisted high-fat-28 diet induced weight gain and diabetes. The metabolic protection in Phospho1 -/mice was manifested in the absence of 29 altered levels of osteocalcin. Osteoblasts isolated from Phospho1 -/mice were enriched for genes associated with 30 energy metabolism and diabetes; Phospho1 both directly and indirectly interacted with genes associated with glucose 31 transport and insulin receptor signalling. Canonical thermogenesis via brown adipose tissue did not underlie the 32 metabolic protection observed in adult Phospho1 -/mice. However, the decreased serum choline levels in Phospho1 -/-33 mice were normalized by feeding a 2% choline rich diet resulting in a normalization in insulin sensitivity and fat mass. 34This study identifies PHOSPHO1 as a potential therapeutic target for the treatment of obesity and diabetes.In addition to its classical structural functions, the skeleton is a site of significant glucose uptake and is involved in the 66 regulation of whole-body glucose metabolism (1-8). Osteocalcin (OCN) is the most abundant osteoblast-specific non-67 collagenous protein derived from bone and is thought to maintain the mechanical properties of the bone matrix by 68 regulating calcium binding when fully carboxylated (GLA13-OCN) (9). However, when OCN is not γ-carboxylated 69 (uncarboxylated (GLU-OCN) or undercarboxylated (GLU13-OCN)), it is released from bone into the circulation where 70 it is able to regulate whole-body glucose metabolism in an endocrine manner (7,(10)(11)(12)(13). Mice deficient in OCN have 71 increased fat mass and are hyperglycemic, hypoinsulinemic and insulin-resistant in muscle. Furthermore, serum GLU17-72 OCN (human form of GLU13) levels and β-cell function show an inverse correlation with glycated haemoglobin 73 (HbA1c), fat mass and plasma glucose levels (14-18). 74 75Osteoblasts regulate glucose metabolism through OCN-dependent and independent mechanisms (19,20).An 76 alternative candidate is the bone-specific cytosolic phosphatase; Phosphatase, Orphan 1 (PHOSPHO1) (21)(22)(23)(24)(25)(26)(27)(28)(29)(30). 77 PHOSPHO1 initiates bone matrix mineralization and PHOSPHO1 deficiency causes significant skeletal pathology, 78 bowed long bones, osteomalacia and scoliosis in early life (31)(32)(33)(34). In addition to the role of PHOSPHO1 in skeletal 79 biomineralization, PHOSPHO1 has been implicated in the regulation of energy metabolism in humans (35)(36)(37)(38). Within 80 the PHOSPHO1 gene, differential methylation sites have been identified as potentially useful biomarkers for clinical 81 application in the early detection of type-2 diabetes (35) and significant associations between methylation at loci within 82 the PHOSPHO1 gene and the future risk of type-2 diabetes exist (36,37). Differential methylation in PHOSPHO1 was 83 associated with three lipid traits (tota...

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“…Uterine decidualization phenomenon has been worsening by DM which contributes in the production of pro-inflammatory uterine RESEARCH ARTICLE condition through generating free radicals leading to embryopathies. Histologically, DM promotes the thinning of uterine myometrium and endometrium (Favaro et al, 2010(Favaro et al, , 2013Usman et al, 2018). Declined smooth muscles with vanished oxytocin contractive myometrium response was also reported in DM.…”

Section: Introductionmentioning

confidence: 99%