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[posted on behalf of CRON4healthyfuture]

Now, I know that message "hunger is good" is not popular in the contemporary feel-good Insant gratification America, but, results are results.

The basic story is this, if you fry a rat's pancreas when a chemical called "streptozocin", they will manifest something that looks just like type 1 diabetes. In other words, no insulin is produced. In response to this, they start eating like there is no tomorrow, and because of that, there really isn't.

What these researchers show is that ghrelin is probably contributing to this effect. In other words, in "insulinoprivic" conditions, or "no insulin conditions", ghrelin goes up, and then you get the munchies.

What does all this mean for the way in which you coordinate a diet? Not sure, but I do find it interesting. There are some arguments for this being something you are supposed to "outsmart", and other arguments for this being something you actually should promote to get the most "benefit".

They further integrated their findings with the current research in Neuropeptide Y to show that ghrelin, a serum protein, uses Neuropeptide Y to induce some of its effects.

The full-text is free........

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Role of endogenous ghrelin in the hyperphagia of mice with streptozotocin-induced diabetes

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"The observation that endogenous plasma ghrelin levels rise shortly before meals
and are rapidly suppressed by food consumption lend credence to the idea that
endogenous ghrelin is a hunger hormone dictating the timing of the meals (8). In addition to short-term fluctuations in ghrelin levels over the course of a day, longer-term regulation of circulating ghrelin appears to occur in relation to body weight change (9,10).

Ghrelin is now considered as the first systemically active orexigenic hormone that
induces weight gain by stimulating an acute increase in food intake as well as by
decreasing fat utilization under conditions of negative energy balance (6,11).
The source of the consumption related feedback that decreases ghrelin levels has not been fully elucidated but absorption of nutrients appears to play an essential role because intragastric infusion of glucose, proteins or fats but not of an equal volume of water lowers ghrelin levels (9,11,12). Williams et al. (13) confirmed that gastric distension and chemosensation do not play a role in the meal-related ghrelin response. It is unclear whether ingested nutrients suppress ghrelin production directly or indirectly, e.g. through insulin, a possibility that is consistent with the reciprocal 24-h profiles of these hormones. This has been confirmed in patients with type I diabetes where absolute insulin deficiency prevented prandial plasma ghrelin suppression until the insulin deficiency was corrected with an intravenous insulin bolus (14). Also in rats with uncontrolled, insulindeficient diabetes induced by the â-cell toxin streptozotocin (STZ), ghrelin levels are increased (
15).
Both conditions are characterized by hyperphagia and it has therefore been suggested that lack of meal-induced ghrelin suppression caused by severe insulin deficiency may explain hyperphagia in uncontrolled type 1 diabetes.

Ishii et al. (15) already showed that treatment with a ghrelin receptor antagonist, D-Lys3-GHRP-6, could partially reverse the diabetic hyperphagia but recent studies questioned the specificity of the ghrelin receptor antagonist (16). At the dosage used D-Lys3-GHRP-6 contracts the fundus of the stomach via activation of 5-HT2B receptors and thereby induces early satiety leading to reduced food intake by impairing gastric accommodation.

The present study therefore aimed to provide conclusive evidence for a role of
endogenous ghrelin in the hyperphagia of mice with uncontrolled insulin deficient
diabetes by comparing food intake in STZ-induced diabetic ghrelin knockout (ghrelin-/-)
mice and their wild type equivalents (ghrelin+/+). For comparison plasma ghrelin levels
and food intake were also studied in STZ-induced diabetic mice treated for 5 days with
either saline or the ghrelin receptor antagonist, D-Lys3-GHRP-6. In both models the
changes in the hypothalamic expression of neurpeptide Y (NPY), á-melanocyte
stimulating hormone (á-MSH) and orexin, neuropeptides known to be involved in the
ghrelin-induced feeding responses were studied (6,17-19)."

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".........These results therefore indicate that NPY is the downstream mediator
of ghrelin in the hyperphagic responses of mice with insulin deficient diabetes."

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http://endo.endojournals.org/cgi/rapidpdf/en.2005-1335v1