I don't really find this that surprising. In animal studies, fructose's claim to fame isn't that it's especially fattening, it's that it induces insulin resistance and type II diabetes. We flinch when a diet that makes rats fat is described as "high fat" when it is also high in sugar--but high sugar in and of itself doesn't make the animals nearly as fat, generally, though it will give them symptoms of metabolic syndrome.
An interesting aspect of this, you see the model of excess fat in adipose, and then spillover to visceral/liver etc. fat then causing insulin resistance, but the liver is involved in various ways with regulation of body fat, there is the possibility that signalling from the liver, or just more constantly elevated insulin levels, makes the adipose tissue less insulin sensitive, so that overall fatness decreases even though insulin is higher.
Stephen Guyunet has a post here;
http://wholehealthsource.blogspot.c...er-nail-in.html
that might relate, he uses it that argue that insulin isn't fattening.
Quote:
In the first study, published in 1980 by Dr. Dennis A. Vanderweele and colleagues, rats were implanted with mini-pumps delivering insulin at a steady rate throughout the day and night for 7 days (4). They tested four different doses: 0, 1, 2 and 6 units per day, and measured food intake and body weight. This is a model of chronically elevated insulin reminiscent of what is seen in insulin-resistant people.
They found that all doses of insulin reduced body weight gain, but only the 2 unit dose was statistically significant. They speculated that the 6 unit dose was less effective at reducing weight gain because it was sufficiently high to cause hypoglycemia (low blood sugar), which is a potent trigger for food intake. Total food intake was suppressed at all doses by insulin as well, but this was apparently not due to illness. The authors conclude:
1) insulin limits meal size when blood levels are modestly elevated for prolonged periods of time in the rat, 2) this decrease in meal size is not compensated for by an increase in meal frequency and, hence, total daily food ingestion and body weight gain are reduced, and 3) this effect appears to be a heightening of satiety rather than an induction of illness.
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Notice the bit about hypoglycemia. If this model induces insulin resistance--I would expect an animal with otherwise normal function would upregulate various counterregulatory hormones pretty much continuously, or downregulate insulin receptors etc., or some combination--a lack of a fattening effect might not be surprising. In contrast, there's a mouse model where inducing hypoglycemia through insulin once a week does induce substantial weight gain.
What happens when an animal eats? Initially, before there's much in the way of nutrient absorption, there's a small initial burst of insulin that serves to reduce nutrients in the blood. You might get this walking by a bakery, suddenly feel hungry. That small burst might be absent if you're insulin resistant--absent or insufficient first phase insulin response figures big in the Newcastle studies. Even a normal insulin response should send a weaker signal if the basal insulin levels are elevated.
Type II patients still getting fatter when they use exogenous insulin makes perfect sense--they're able to add enough to blast past the resistance, perhaps it's more the large boluses for meals that's fattening rather than the basal insulin.