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Erica Yeo
Erica Yeo
Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
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Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
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Patricia L Brubaker
Patricia L Brubaker
Department of Physiology, University of Toronto, Toronto, ON, Canada
Department of Medicine, University of Toronto, Toronto, ON, Canada
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Department of Medicine, University of Toronto, Toronto, ON, Canada
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Deborah M Sloboda
Deborah M Sloboda
Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
Department of Obstetrics, Gynecology and Pediatrics, McMaster University, Hamilton, ON, Canada
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Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
Department of Obstetrics, Gynecology and Pediatrics, McMaster University, Hamilton, ON, Canada
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resistance which drives maternal β-cells to synthesize and secrete more insulin. This expansion of insulin-producing β-cells coincides with the onset of PL, PGH and prolactin (PrL) secretion from the placenta. As PL, PGH and PrL induce β-cell proliferation
