The study is the first to describe how ladies b**bs becomes highly sensitive to:
Insulin during lactation. It is also the first study to get an
accurate picture of how specific genes are switched on in the human
mammary gland during lactation.The researchers used next generation
sequencing technology, RNA sequencing, to reveal “in exquisite detail”
the blueprint for making milk in the human mammary gland, according to
Laurie Nommsen-Rivers, PhD, RD, IBCLC, a scientist at Cincinnati
Children’s and corresponding author of the study, published online in
PLOS ONE, a journal of the Public Library of Science.
Nommsen-Rivers’ previous research had shown that for mothers with
markers of sub-optimal glucose metabolism, such as being overweight,
being at an advanced maternal age, or having a large birth-weight baby,
it takes longer for their milk to come in, suggesting a role for insulin
in the mammary gland. The new research shows how the mammary gland
becomes sensitive to insulin during lactation.
For a long time, insulin was not thought to play a direct role in regulating the milk-making cells of the human bréast, because insulin is not needed for these cells to take in sugars, such as glucose. Scientists now, however, appreciate that insulin does more than facilitate uptake of sugars.
“This new study shows a dramatic switching-on of the insulin receptor and its downstream signals during the bréast’s transition to a bio factory that manufactures massive amounts of proteins, fats and carbohydrates for nourishing the newborn baby,” says Dr. Nommsen-Rivers.
“Considering that 20 per cent of women between 20 and 44 years old
are pre-diabetic, it’s conceivable that up to 20 per cent of new mothers
in the United States are at risk for low milk supply due to insulin
dysregulation.”
Dr. Nommsen-Rivers and her colleagues were able to use a non-invasive method to capture mammary gland RNA — a chain of molecules that are blueprints for making specified proteins — in samples of human bréast milk. They then created the first publicly accessible library of genes expressed in the mammary gland based on RNA-sequencing technology.
This approach revealed a highly sensitive portrait of the genes being expressed in human milk-making cells. They discovered an orchestrated switching on and off of various genes as the mammary gland transitions from secreting small amounts of immunity-boosting colostrum in the first days after giving birth to the copious production of milk in mature lactation.
In particular, the PTPRF gene, which is known to suppress intracellular signals that are usually triggered by insulin binding to its receptor on the cell surface, may serve as a biomarker linking insulin resistance with insufficient milk supply. These results lay the foundation for future research focused on the physiological contributors to mothers’ milk supply difficulties.
Now that they’ve demonstrated the significance of insulin signalling in the human mammary gland, they are planning a phase I/II clinical trial with a drug used to control blood sugar in type 2 diabetes to determine whether it improves insulin action in the mammary gland, thus improving milk supply. While a drug is not an ideal way to solve the problem of sub-optimal glucose metabolism impairing bréastfeeding, according to Dr. Nommsen-Rivers, it is excellent for establishing proof-of-concept through the use of a placebo controlled randomized clinical trial.
“The ideal approach is a preventive one,” she says. “Modifications in diet and exercise are more powerful than any drug. After this clinical trial, we hope to study those interventions.”
Source: Science Daily
For a long time, insulin was not thought to play a direct role in regulating the milk-making cells of the human bréast, because insulin is not needed for these cells to take in sugars, such as glucose. Scientists now, however, appreciate that insulin does more than facilitate uptake of sugars.
“This new study shows a dramatic switching-on of the insulin receptor and its downstream signals during the bréast’s transition to a bio factory that manufactures massive amounts of proteins, fats and carbohydrates for nourishing the newborn baby,” says Dr. Nommsen-Rivers.
Dr. Nommsen-Rivers and her colleagues were able to use a non-invasive method to capture mammary gland RNA — a chain of molecules that are blueprints for making specified proteins — in samples of human bréast milk. They then created the first publicly accessible library of genes expressed in the mammary gland based on RNA-sequencing technology.
This approach revealed a highly sensitive portrait of the genes being expressed in human milk-making cells. They discovered an orchestrated switching on and off of various genes as the mammary gland transitions from secreting small amounts of immunity-boosting colostrum in the first days after giving birth to the copious production of milk in mature lactation.
In particular, the PTPRF gene, which is known to suppress intracellular signals that are usually triggered by insulin binding to its receptor on the cell surface, may serve as a biomarker linking insulin resistance with insufficient milk supply. These results lay the foundation for future research focused on the physiological contributors to mothers’ milk supply difficulties.
Now that they’ve demonstrated the significance of insulin signalling in the human mammary gland, they are planning a phase I/II clinical trial with a drug used to control blood sugar in type 2 diabetes to determine whether it improves insulin action in the mammary gland, thus improving milk supply. While a drug is not an ideal way to solve the problem of sub-optimal glucose metabolism impairing bréastfeeding, according to Dr. Nommsen-Rivers, it is excellent for establishing proof-of-concept through the use of a placebo controlled randomized clinical trial.
“The ideal approach is a preventive one,” she says. “Modifications in diet and exercise are more powerful than any drug. After this clinical trial, we hope to study those interventions.”
Source: Science Daily
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