glucose receptors are found in any cells of the body, even in the fat cells compartment. it's sure that you'll find very old paper relating that those cells were not consuming glucose but since it's the source of so many pathways (even for fat metabolism) there is no way that glucose is not metabolized by fat cells. of course it's simple in healthy cells and bodies, but hormones and metabolisms deregulations in insulin resistance, T2D and obesity will change the rules. you can dig in boomed, but there are lot of papers.
The insulin target Glut4 is the transporter involved in glucose uptake by adipocytes. Glycolysis is absolutely required to generating the 3C precursor of the glycerol to which fatty acids are linked in triglycerides. You can find relevant information about this in most Biochemistry textbooks.
Glucose entry into cells is facilitated by a family of ubiquitously expressed glucose transporter proteins. Glucose transporters are localized on the plasma membrane. Exception is the Glut4, which is specifically expressed in insulin sensitive tissues, i.e., skeletal muscle, heart muscle, and fat and is responsible for the insulin effect on blood glucose clearance. Under basal conditions, Glut4 is compartmentalized in intracellular membrane vesicles and thus has no access to the extracellular space. Upon insulin administration, Glut4-containing vesicles fuse with the plasma membrane and deliver the transporter to its site of action. As a result, Glut4 content on the plasma membrane is increased, and glucose uptake in the cell is significantly elevated.
So glycerol can not enter fat cell? It needs to be build by glycolysis? Or is it an extra pathway? In general some people seem to claim glucose can not be transfered into fat. Of course maybe that is different (glucose to fat versus glucose in fat cells in glycolysis).
Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation. This glycerol is instead shuttled to the liver via the blood where it is phosphorylated by glycerol kinase to glycerol 3-phosphate. Glycerol 3-Phosphate converted to dihydroxyacetone phosphate (DHAP) via Glycerol 3-Phosphate Dehydrogenase. DHAP can participate in glycolysis or gluconeogenesis.
In the fat cells, induction of peroxisome proliferator-activated receptor up-regulates adiponectin (a proinsulin-sensitizing adipokine) and glucose transporter (Glut)1 and Glut4 (cellular Glut responsible for glucose uptake), and enhances glucose uptake