plasma glucagon and intestinal mass seen in untreated diabetes.”  

But the insufficient insulin causes the small intestines to produce additional glucose when insufficient hormone has been supplied. Not only does the body need insulin to use food for fuel, the body is triggering a survival mechanism, which works against the diabetic. The scientific community refers to this survival stimulated glucose as endogenous glucose production (EGP). In the copyrighted American Diabetes Association 2001 article, “Rat Small Intestine Is an Insulin-Sensitive Gluconeogenic Organ” the authors Martine Croset, Fabienne Rajas, Carine Zitoun, Jean-Marc Hurot, Sandrine Montano, and Gilles Mithieux with the Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine R.T.H. Laennec, Lyon, France, provided the following conclusion.

This organ is insulin sensitive as well as the kidneys. In  fact a majority of the kidney transplant patients are diabetics also.

“We show here that, at variance with the current view that only the liver and the kidney are glucose-producing organs, small intestine contributes 20–25% of systemic EGP in (emergency glucose) in rats. In addition, small intestine (blood sugar) production may be suppressed by insulin.”

As has been demonstrated above, the high blood sugar causes organ damage and dysfunction. The kidneys also suffer from the diabetic state.

The incidence of end-stage (kidney) disease (ESRD) is increasing worldwide. In the United States alone, there were 372,000 patients requiring renal (kidney transplant) replacement therapy in the year 2000 and is expected to rise to 650,000 by the year 2010,” © 2002 American Society of Nephrology.  

“The most obvious effect of diabetes was enlargement of the kidney. As shown, the increase in kidney size was evident in both the renal cortex and medulla,” according to the authors Shirong Zheng¹, William T. Noonan², Naira S. Metreveli¹, Susan Coventry³, Patricia M. Kralik¹, Edward C. Carlson⁴, and Paul N. Epstein¹  In the article Development of Late-Stage Diabetic Nephropathy in OVE26 Diabetic Mice,  © 2004 by the American Diabetes Association, Inc. the authors concluded a low protein diet and keeping the glucose well controlled is helpful. In the article, “Halting the Progression of Chronic Nephropathy “ the authors Ruth C. Campbell*, , Piero Ruggenenti*, and Giuseppe Remuzzi the authors concluded: “However, most authorities recommend intensified glucose control as a strategy to slow microvascular and macrovascular complications.