Publications by authors named "J K Kruit"

Gestational diabetes mellitus (GDM) is associated with increased postpartum risk for metabolic dysfunction-associated steatotic liver disease (MASLD). GDM-related MASLD predisposes to advanced liver disease, necessitating a better understanding of its development in GDM. This preclinical study evaluated the MASLD development in a lean GDM mouse model with impaired insulin secretion capacity.

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Age is the greatest risk factor for the development of type 2 diabetes mellitus (T2DM). Age-related decline in organ function is attributed to the accumulation of stochastic damage, including damage to the nuclear genome. Islets of T2DM patients display increased levels of DNA damage.

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Cancer survivors who received chemotherapy, such as the anthracycline doxorubicin (DOX), have an increased risk of developing complications later in life, including the development of chronic metabolic diseases. Although the etiology of this increased risk for late metabolic complications in cancer survivors is poorly understood, a causal role of therapy-induced senescent cells has been suggested. To study the role of cellular senescence in chemotherapy-induced metabolic complications, young adult female low-density lipoprotein receptor-deficient (Ldlr)-p16-3MR mice, in which p16-positive (p16) senescent cells can be genetically eliminated, were treated with four weekly injections of DOX (2.

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Hyperglycaemia in pregnancy (HIP) is a pregnancy complication characterized by mild to moderate hyperglycaemia that negatively impacts short- and long-term health of mother and child. However, relationships between severity and timing of pregnancy hyperglycaemia and postpartum outcomes have not been systemically investigated. We investigated the impact of hyperglycaemia developing during pregnancy (gestational diabetes mellitus, GDM) or already present pre-mating (pre-gestational diabetes mellitus, PDM) on maternal health and pregnancy outcomes.

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Article Synopsis
  • FGF1 is a growth factor released from fat tissue that plays a role in regulating glucose uptake during changes in nutrition.
  • Research showed that FGF1 enhances glucose uptake in fat cells (adipocytes) through the activation of the GLUT4 transporter, relying on certain signaling proteins (MEK1/2 and Akt).
  • Prolonged exposure to FGF1 also increases glucose uptake by promoting the transcription of GLUT1, suggesting a new, insulin-independent pathway that could be useful in treating type 2 diabetes.
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