Question

Biochemistry.

Judging by this graph, which shows the results of a research study demonstrating the varying differences in glycemic responses to foods among individuals, what is a possible biological reason for these differences? What pathway could be altered between individuals?

Does this have anything to do with mTOR or the insulin receptor signaling pathway? I dont know what could be the reasoning behind this graph.

Blood glucose (mg/dl) 240 L Individual PPGRs to bread Mean iAUC (mg/dl.h) Participant AUC = 139 67 663 637 358 FAUC = 81 ¡AUC = 44 AUC = 15 80 0 | 20 100 120 40 60 80 Time (min)

Answer 1

Answer:

The food used here is constant for all 4 individuals.

Also the 2 values for each individual is comparable.

All graphs start in 80-120 range.

Post prandial insulin and glucose activate mTor within metabolic tissues. Which in turn plays important role in glucose and lipid metabolism.

mTor is otherwise called rapamycin and its downstream target S6 kinase is involved in aminoacid induced insulin resistance.

The most important stimulus for insulin production is post prandial increase of blood sugar levels.

Insulin mediates transport of glucose into the cell by translocation of glucose transporter(GLUT4) from intra cellular pool to plasma membrane.

This occurs through multiple steps of PI3K/AKT pathway and protein kinase B.

The difference in values also has got connection with beta cell mass in pancreas. Which in turn dependent on growth hormone, prolactin, placental lactogen and GLP1.

Insulin RTK is responsible for insulin secretion in response to glucose levels. PKB gets activated and phosphorylate GSK3beta. Glycogen Synthase is activated so that UDP glucose turns to glycogen.ISPK activate PP1. inhibiting glycogen break down.

From individual to individual there will be differences in beta cell mass in pancreas, different body mass index, presence of central obesity or an error in any of above pathways, insulin resistance can affect and change post prandial glucose levels.

Inflammasomeand oxidative stress lead to IL1beta secretion which impart insulin resistance.