I used to think the same way too, but it's not. Just because it's in the New York Times' Magazine doesn't mean it's not true.
"The phrase Lustig uses when he describes this concept is 'isocaloric but not isometabolic.' This means we can eat 100 calories of glucose (from a potato or bread or other starch) or 100 calories of sugar (half glucose and half fructose), and they will be metabolized differently and have a different effect on the body. The calories are the same, but the metabolic consequences are quite different."
Fructose, insulin resistance, and metabolic dyslipidemia
Figure 2, "Hepatic fructose metabolism: A highly lipogenic pathway," does a good job showing the pathway.
"Fructose is readily absorbed from the diet and rapidly metabolized principally in the liver. Fructose can provide carbon atoms for both the glycerol and the acyl portions of triglyceride. Fructose is thus a highly efficient inducer of de novo lipogenesis. High concentrations of fructose can serve as a relatively unregulated source of acetyl CoA. In contrast to glucose, dietary fructose does NOT stimulate insulin or leptin (which are both important regulators of energy intake and body adiposity). Stimulated triglyceride synthesis is likely to lead to hepatic accumulation of triglyceride, which has been shown to reduce hepatic insulin sensitivity, as well as increased formation of VLDL particles due to higher substrate availability, increased apoB stability, and higher MTP, the critical factor in VLDL assembly."
When I went to med school, 1987 - 91, there was no mention of non-alcoholic fatty liver disease, NAFLD. There is now, including in kids. Check out the keyword nafld.
I checked out high fructose corn syrup. HFCS-55, the version used in soft drinks, is 55 % fructose, 42 % glucose and 3 % other sugars. 56/42 is the same as 4/3. You're getting almost 4 molecules of fructose for every 3 molecules of glucose with HFCS-55.