Mathematical model of diabetes and lipid metabolism linked to diet, leptin sensitivity, insulin sensitivity and VLDLTG clearance predicts paths to health and type II diabetes

Oct 19, 2019Journal of theoretical biology

Mathematical model shows how diet, hormone responses, and fat processing affect diabetes risk and health

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Abstract

The model predicts isocaloric high carbohydrate low fat (HCLF) and low carbohydrate high fat (LCHF) diet trajectories vary in fat mass by at most a few kilograms at steady state.

LCHF diet trajectories to health are predicted to be faster for fat mass loss compared to HCLF trajectories.
Leptin sensitivity and clearance of very low density lipoprotein triglyceride (VLDLTG) are thought to increase on low carbohydrate diets.
Increased leptin sensitivity and VLDLTG clearance could lead to lower fat mass and VLDLTG levels.
Changes in VLDLTG due to dietary changes are predicted to occur rapidly, reaching steady state values in a few weeks.
If only insulin sensitivity increases on a low carbohydrate diet, fat mass may slightly increase.
Simultaneous increases in leptin and insulin sensitivities could result in fat mass decrease.

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An original model of diabetes linked to carbohydrate and lipid intake is presented and applied to predict the effects on biomarkers of various diets. The variables (biomarkers) are concentrations of fasting plasma glucose, insulin, leptin, glucagon, non-esterified fatty acids (NEFA) and very low density lipoprotein triglyceride (VLDLTG), as well as muscle lipids, hepatic lipids, pancreatic lipids, fat mass and mass of β-cells. The model predicts isocaloric high carbohydrate low fat (HCLF) diet and low carbohydrate high fat (LCHF) diet trajectories to health which vary in fat mass by at most a few kilograms at steady state. The LCHF trajectories to health are faster than isocaloric HCLF trajectories with respect to fat mass loss, although these trajectories may be slower initially if parameters are adjusting from HCLF values. On LC diets, leptin sensitivity and VLDLTG clearance are thought to increase. Increasing leptin sensitivity and VLDLTG clearance is predicted to lower lipids including fat mass and VLDLTG. The model predicts that changes in VLDLTG due to a change in diet happen rapidly, approaching steady state values after a few weeks, reflecting leptin sensitivity and VLDLTG clearance which are much harder to measure. The model predicts that if only insulin sensitivity increases on a LC diet, steady state fat mass would increase slightly. If leptin and insulin sensitivities increase concurrently, the combined effect could be a decrease in fat mass, consistent with the fact that increasing insulin sensitivity is often associated with fat mass loss in trials. The model predicts trajectories to fat type II diabetes with hypertriglyceridemia due to high carbohydrate moderate fat diets, on which insulin rises before falling, as ectopic fat deposits increase; made fatter and more diabetic by higher lipid consumption. It predicts trajectories to non-diabetic states with raised fat mass, VLDLTG and muscle, hepatic and pancreatic lipids due to moderate carbohydrate high fat diets. The model predicts paths to lean type II diabetes, on a diet of moderate energy but low β-cell replication rate or high death rate.

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Mathematical model of diabetes and lipid metabolism linked to diet, leptin sensitivity, insulin sensitivity and VLDLTG clearance predicts paths to health and type II diabetes

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