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Role of resistin in milk synthesis and tight junction formation in cellular models of lactation

Taha Elajnaf, University of Oxford



Obesity and diabetes are major causes of lactation insufficiency, which affects ~10% of breastfeeding women. However, the underlying mechanisms remain unclear. Resistin, a pro-inflammatory hormone which is elevated in obesity and diabetes, may potentially contribute to lactation insufficiency. In support of this, our lab has demonstrated by in silico transcriptomic analysis that cyclase associated protein (CAP1), a resistin receptor, is highly expressed in the human mammary gland during lactation. CAP1 has been reported to inhibit milk synthesis in bovine mammary cells. Moreover, resistin has been reported to downregulate tight-junction proteins in human mammary epithelial cancer cells. These tight-junction proteins initiate milk secretion in the early postpartum period.  

The involvement of the resistin-CAP1 axis in human lactation is yet to be characterised. In order to address this gap, I aim to undertake the following studies:

  1. Evaluate the expression of CAP1 in a range of mammary gland cell types at the RNA and protein level.
  2. Assess the effects of resistin on milk protein synthesis and tight junction formation in human mammary epithelial cells stimulated with lactogenic hormones.


Grant awarded: £1,993.00

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