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Vitamin and mineral deficiencies which may predispose to glucose intolerance of pregnancy
- Source :
- Journal of the American College of Nutrition. 15:14-20
- Publication Year :
- 1996
- Publisher :
- Informa UK Limited, 1996.
-
Abstract
- There is an increased requirement for nutrients in normal pregnancy, not only due to increased demand, but also increased loss. There is also an increased insulin-resistant state during pregnancy mediated by the placental anti-insulin hormones estrogen, progesterone, human somatomammotropin; the pituitary hormone prolactin; and the adrenal hormone, cortisol. If the maternal pancreas cannot increase production of insulin of sustain normoglycemia despite these anti-insulin hormones, gestational diabetes occurs. Gestational diabetes is associated with excessive nutrient losses due to glycosuria. Specific nutrient deficiencies of chromium, magnesium, potassium and pyridoxine may potentiate the tendency towards hyperglycemia in gestational diabetic women because each of these four deficiencies causes impairment of pancreatic insulin production. This review describes the pathophysiology of the hyperglycemia and the nutrient loss in gestational diabetes and further postulates the mechanism whereby vitamin/mineral supplementation may be useful to prevent or ameliorate pregnancy-related glucose intolerance.
- Subjects :
- Chromium
Glycosuria
medicine.medical_specialty
medicine.medical_treatment
Medicine (miscellaneous)
Somatomammotropin
Pregnancy
Diabetes mellitus
Magnesium deficiency (medicine)
Internal medicine
medicine
Humans
Potassium Deficiency
Nutrition and Dietetics
business.industry
Insulin
medicine.disease
Pregnancy Complications
Gestational diabetes
Diabetes, Gestational
Endocrinology
Female
medicine.symptom
Vitamin B 6 Deficiency
business
Magnesium Deficiency
Hormone
Subjects
Details
- ISSN :
- 15411087 and 07315724
- Volume :
- 15
- Database :
- OpenAIRE
- Journal :
- Journal of the American College of Nutrition
- Accession number :
- edsair.doi.dedup.....01d0159cc5c755a6a15cac58f190ecf5
- Full Text :
- https://doi.org/10.1080/07315724.1996.10718560