Answer :
On the short term, glucagon promotes glycogenolysis, increasing hepatic glucose synthesis through nontranscriptional mechanism(s), but it may also impact components required for gluconeogenesis and glycogenolysis through transcriptional activation of CREB.
It has been demonstrated that the presence of phosphoenolpyruvate carboxykinase (PEP carboxykinase) and a few other gluconeogenic enzymes allows pyruvate to be converted to glycerol 3-P in both adipocytes and hepatocytes. A metabolic process called glyceroneogenesis produces glycerol 3-phosphate or triglycerides from sources other than glucose.
Glycolysis typically produces glycerol 3-phosphate from glucose, but when the cytosolic content of glucose decreases, a different route known as glyceroneogenesis is used to produce it. Therefore, glycerol 3-phosphate must be produced from either glycogen that has been stored, incoming plasma glucose, or pyruvate since glycerol cannot act as a precursor for TG production in adipose tissue. Glycerol kinase changes glycerol into glycerol-3-phosphate, which can then be broken down by cytosolic (and/or mitochondrial) glycerol 3-phosphate dehydrogenase into dihydroxyacetone phosphate.
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