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And high intakes of trans fats may cause insulin resistance, a marker of type 2 diabetes.
Alternatively, increased lipotoxicity may cause insulin resistance.
More specifically, intramyocellular sphingolipids may cause insulin resistance by disrupting insulin signaling pathways in the muscle [31].
These in vitro observations support the hypothesis that lower extracellular pH may cause insulin resistance in skeletal muscle cells.
Increasing evidence suggests that loss of β cell characteristics may cause insulin secretory deficiency in diabetes, but the underlying mechanisms remain unclear.
The insulin signal cascades, which include PKB/Akt through PI3K and mTOR, stimulate S6K1, resulting in a negative feedback, which may cause insulin resistance [ 55, 56].
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One mechanism is the related to the higher protein/nitrogen content of infant formula compared with breast milk, which may cause increased insulin and insulin-like growth factor-1 secretion leading to excessive weight gain [ 15].
Here, we hypothesize that sympathetic activation may cause peripheral insulin resistance defined as partial blocking of insulin effects on glucose uptake.
Friedman et al. (1993) suggested that the lack of PEPCK gene expression may cause defective insulin signaling and induce hyperglycemia in diabetic animal models.
Obesity often cause insulin resistance, which may promote the development of breast cancer [ 46, 47].
Because the activation of inflammatory pathways may downregulate insulin signaling which can cause insulin resistance, vitamin D might impact the risk of diabetes through the inflammatory response [ 8– 14].
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