Lipid Metabolism - Fatty acid synthesis

I have covered lipid metabolism and fatty acid synthesis. I mentioned the following statements:

Recall

1. Fatty acid synthesis occurs in the cytosol (as opposed to nucleus or mitochondria).
2. Acetyl CoA carboxylase (ACC) is a part of the large multienzyme fatty acid synthase complex.
3. ACC is responsible for producing malonyl CoA, the first step in fatty acid synthesis. 
4. Fatty acid synthesis requires 2 things - acetyl CoA and NADPH.
5. Where do acetyl CoA and NADPH come from?
6. Acetyl CoA comes from the Kreb cycle, from the mitochondrial matrix
7. NADPH comes from the pentose phosphate pathway (PPP).
8. Acetyl CoA needs to exit the mitochondria and enter into the cytosol, where fatty acid synthesis can then occur.
9. More two-carbon (2C or C2) units are added in subsequent steps, till the fatty acyl chain has 16 carbons (16C), which is palmitic acid (C16:0). Palmitic acid has no carbon double bonds (C=C) because it is a saturated fatty acid. Only palmitic acid is formed.

Reading

Please read this scientific journal article at NIH Public Access:
Michael J. MacDonald, Agnieszka Dobrzyn, James Ntambi, and Scott W. Stoker
Arch Biochem Biophys. 2008 February 15; 470(2): 153–162.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453002/pdf/nihms40601.pdf

Pancreatic beta cell mitochondria convert insulin secretagogues into products that support insulin exocytosis. We explored the idea that lipids are some of these products formed from acyl group transfer out of mitochondria to the cytosol, the site of lipid synthesis. There are two isoforms of acetyl-CoA carboxylase, the enzyme that forms malonyl-CoA from which C2 units for lipid synthesis are formed. We found that ACC1, the isoform seen in lipogenic tissues, is the only isoform present in human and rat pancreatic islets [...]. Inhibitors of ACC and fatty acid synthase inhibited insulin release in islets [...]. Carbon from glucose and pyruvate were rapidly incorporated into many lipid classes in INS-1 cells. Glucose and other insulin secretagogues acutely increased many lipids with C14-C24 chains including individual cholesterol esters, phospholipids and fatty acids. Many phosphatidylcholines and phosphatidylserines were increased and many phosphatidylinositols and several phosphatidylethanolamines were decreased. The results suggest that lipid remodeling and rapid lipogenesis from secretagogue carbon support insulin secretion.- MacDonald et al, ABB 2008, 470(2):153-162.

Further study notes

1. There are 2 isoforms of ACC.
2. Lipogenic tissues contain ACC1 isoform.
3. ACC1 is found in human and rat pancreatic islets.
4. Inhibitors of ACC and fatty acid synthase inhibited insulin release in pancreatic islets.
5. Glycolysis: each glucose molecule has 6 carbons; each pyruvate molecule has 3 carbons.
6. Carbon (C) from glucose and pyruvate were rapidly incorporated into many lipid classes.
7. Glucose and other insulin secretagogues increased C14-C24 lipid chains in 3 lipid classes - cholesteryl esters, phospholipids and fatty acids.
8. Comparing the 4 phospholipids (PLs) classes, many phosphatidylcholines (PCs) and phosphatidylserines (PSs) were increased and many phosphatidylinositols (PIs) and several phosphatidylethanolamines (PEs) were decreased.
9. Triglyceride (TG) synthesis shares the same pathway (at some point) with phospholipid synthesis.
10. Diphosphatidate can go to form either TG or PL. 

Further questions

1. Where are the other fatty acids (C14, C12, C10, C8, C4) formed?
2. Are any of them important?