Pancreatic β-cells and skeletal muscle act in a synergic way in the control of systemic glucose homeostasis.
Several pyruvate-dependent and pyruvate-independent shuttles increase tricarboxylic acid cycle intermediate anaplerosis and increase β -cell ATP:ADP ratio, triggering insulin exocytotic mechanisms.
Mitochondrial tricarboxylic acid cycle intermediate cataplerosis gives rise to the so-called metabolic coupling factors, which are also related to insulin release.
Peripheral insulin resistance seems to be related to skeletal muscle fatty acid accumulation and oxidation imbalance. Exercise increases skeletal muscle tricarboxylic acid cycle intermediate anaplerosis, increasing fatty acid oxidation and restores insulin sensitivity.
Protein malnutrition reduces β -cell insulin synthesis, release and peripheral sensitivity. Despite little available data concerning mitochondrial metabolism under protein malnutrition, evidence points towards reduced β-cell and skeletal musc1e mitochondrial capacity.
The observed decrease in insulin synthesis and release may reflect reduced anaplerotic and cataplerotic capacity.
Furthermore, insulin release is tightly coupled to ATP:ADP increase which in turn is related to tricarboxylic acid cycle intermediate anaplerosis. The effect of protein malnutrition upon peripheral insulin resistance is time-dependent and directly related to fatty acid oxidation capacity. In contrast to β-cells, tricarboxylic acid cycle intermediate anaplerosis and cataplerosis pathways in skeletal muscle seem to control fatty acid oxidation and regulate insulin resistance.
Zoppi et al 2010 Insulin release, peripheral insulin resistance and muscle function in protein malnutrition: a role of tricarboxylic acid cycle anaplerosis. British Journal of Nutriton vol 103, 1237-1250

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