When the study for this web site started some years ago, we assumed that the problem of Obesity, as an issue in Hyperinsulinemia and Type II diabetes, was one that was relatively well understood and thoroughly researched. We were surprised to discover that less is known about the weight control mechanism, the hunger reflex and their relationship to Hyperinsulinemia than is known about vitually any other aspect of this dangerous disease.

During our research we found many competing theories with various credibility levels. The best of them, though incomplete, made sense and came from some of the most reputable research labs around the world; the worst of them made no sense at all and typically originated in the sales departments of the diet and weight loss industry.

We present here that which we think makes the most sense and which will likely remain as a basic fundamental to a full understanding of Obesity, if and when it ever becomes available.

With Hyperinsulinemia, the excess average Insulin levels experienced cause an increase of Lipogenesis. Lipogenesis is the Insulin mediated conversion of Glucose into Triglycerides (fats). The resulting high Serum Triglycerides are stored in adipose cells throughout the body; these adipose (fat) cells become distended and as they distend, more Insulin is required to enable them to carry on their metabolic processes. There is but a finite, fixed number of fat cells available in each body. This number is changed only with difficulty as we mature. The excess Triglyceride load that they absorb in Obesity simply makes each adipose cell larger.

As these fat cells absorb the excess Triglyceride load, they emit a biochemical into the blood stream called Leptin. This is a biochemical that causes a reduction in the amount of a Neural Polypeptide called NPY (neural polypeptide Y) which is produced in the Hypothalamus. The Hypothalamus is the part of our brain known to mastermind many of the bodies regulatory mechanisms. The body weight seems to depend upon the ratio of Leptin, emitted by the fat cells, and NPY produced by the Hypothalamus. When there is too much NPY, and possibly other more obscure Neural Peptides, Glucose transfer into the cells is inhibited, Lipogenesis is stimulated and Triglycerides are stored in fat cells. When there is too much Leptin, fat storage is supposed to be inhibited.

This same Hypothalamus also masterminds the control of the Appestat (hunger regulator). The role of NPY and Leptin, if any, in the hunger reflex is not well understood yet. But, clearly there is a connection because the only way to provide the additional Triglyceride load for the fat cells to store is to stimulate the hunger reflex to require more eating of carbohydrates and of fats and oils.

In the case of Obesity, the NPY and Leptin levels remain elevated and it appears that the appropriate Leptin receptors in the Hypothalamus are desensitized. The result is that the Hypothalamus continues to insist upon Triglyceride storage in the adipose cells, by emitting NPY, and it continues to maintain a hunger reflex beyond any reasonable need to do so. We get fat.

One theory, which has some epidemiological support, may be helpful. It says that because the food we eat is so empty of needed nutrients, our hunger reflex remains activated and the role of Leptin remains suppressed. This is done in the body's expectation that, if we continue to eat, eventually the needed nutrient will magically appear in the stomach. The assumption here is that when the needed nutrient appears, the Leptin-NPY axis will again function and we will lose weight. This theory may be fruitful in the effort to more fully understand the connection between the Hypothalamus, which is widely considered to be a lower center control mechanism, and the higher centers of our brain where our intelligence resides.

At any event, while the connection between Obesity and Hyperinsulinemia, is not yet fully understood, much more is known about the cause, progress and cure of Hyperinsulinemia and Type II diabetes.

For those who would like to pursue the study of Obesity beyond these meager beginnings we include a starter reference list. Judicious use of it can quickly get you into the mainstream of what's going on worldwide in this area. More data is included in our Special Report on the Hyperinsulinemia that is so often causal in our Obesity and weight control issues.


  1. Boden G, "Free Fatty Acids, Insulin Resistance, and Type 2 Diabetes Mellitus." Proc Assoc Am Physicians 1999 May9;111(3):241-248
  2. Jeanrenaud B, et al, "[From Claude Bernard to the regulatory system between the hypothalamus and the periphery: implications for homeostasis of body weight and obesity]." C R Seances Soc Biol Fil 1998;192(5):829-841
  3. Stejskal D, et al, "[leptin, insulin and proinsulin--their relationship]." Vnirt Lek 1998 Jun;44(6):361-365
  4. Koyama K, et al, "Tissue triglycerides, insulin resistance, and insulin production: implications for the hyperinsulinemia of obesity." Am J Physiol 1997 Oct;273(4Pt):E708-13
  5. Rohner-Jeanrenaud E, Jeanrenaud B, "Central nervous system and body weight regulation.", Ann Endocrinol (Paris) 1997;58(2):137-142

Return to home page