Insulin level

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Thiazolidinediones (PPARy-agonists) Thiazolidine-diones ( pioglitazone, rosiglitazone) lower blood glucose levels in animal models of insulin resistance and also in insulin resistant patients. They are agonists of the peroxisome proliferator-activated receptor y (PPARy). Because they enhance the effect of insulin and reduce serum insulin levels in insulin resistant patients, thiazolidinediones are usually referred to as insulin sensitizers . 

Metformin sensitizes die liver to circulating insulin levels and reduces hepatic glucose production. 

Sorbitol is a sugar alcohol. It has two thirds the calories of sugar, and is only 60 percent as sweet. It is poorly absorbed by the body, so it does not raise insulin levels as much as sugar. It does not promote tooth decay. 

SCHWARTZ J G, GUAN D, GREEN G M, PHILLIPS w T (1994) Treatment with an oral proteinase inhibitor slows gastric emptying and acutely reduces glucose and insulin levels after a liquid meal in type 11 diabetic patients. Diabetes Care. 17 255-62. 

Figure 12. Minimum serum glucose levels (a) and maximum serum insulin levels (b) as a function of time after the last treatment with 54IU insulin, b.i.d., for nine days.

Conjunctival insulin absorption in rabbits estimated as plasma insulin levels after punctal occlusion was also shown to be increased by bile salts (sodium deoxycholate, glycocholate, and taurocholate) and a surfactant (polyoxyethylene-9-lauryl ether) [200], Their rank order of effectiveness at 1% was sodium deoxycholate > polyoxyethylene-9-lauryl ether > sodium glycocholate = sodium taurocholate. There was an 18-, 29-, 3-, and 3-fold increase, respectively, in conjunctival absorption. Sodium deoxycholate, a dihydroxy bile salt, was more effec-... 

A few hours after eating, the supply of easily available nutrients has been used up and stores must be mobilized to maintain relatively constant supplies of energy and glucose (Fig. 17-7). Insulin levels drop and glucagon levels rise. Because of the increased glucagon levels, cAMP levels rise and regulated proteins become more phosphorylated. 

Although infusion pumps can go some way towards mimicking normal control of blood insulin levels, transplantation of insulin-producing pancreatic cells should effectively cure the diabetic patient, and research aimed at underpinning this approach continues. 

After 48 h, marked increase in blood glucose, depressed plasma insulin level, marked depletion of liver glycogen, significant increase in plasma creatinine phosphokinase and glutamic oxaloacetic transaminase activity (Giri etal. 1979)... 

This paper summarizes our evidence that the mechanism involves protein stimulation of insulin secretion, followed rapidly by insulin inhibition of renal calcium reabsorption. In humans, urinary calcium was proportional to peak postprandial insulin levels in several experiments, after either protein or sucrose was fed. 

In rats, infusion of the insulin secretagogues arginine and glucose induced a calciuria proportional to serum insulin levels. Suppression of insulin secretion by mannoheptulose or streptozotocin prevented the calciuria. Parathyroidectomy did not affect arginine-induced hypercalciuria in the rat, so insulin is not inhibiting parathyroid hormone secretion or activity. 

Figure 2. Peak serum insulin levels vs postprandial urine calcium excretion after a sucrose load.

Figure 3. Regression of plasma insulin levels against urinary calcium excretion for animals in all treatment groups.

The above experiments strongly suggest to us that a linear relationship exists between serum or plasma insulin levels over a wide physiological range, and urinary calcium excretion. The calciuric response to arginine or glucose infusion does not occur if insulin secretion is prevented, as evidenced by the data obtained from animals made acutely insulinopenic by mannoheptulose, or more chronically diabetic by streptozotocin. 

Table II. Postprandial Effects of Diet on Serum Insulin Levels...

Another form of diabetes is non-insulin-dependent diabetes mellitus (NIDDM, or adult diabetes, or type II diabetes). In this case, insulin is produced and a normal insulin level is detected in blood. But for various reasons its effect is reduced. This may be caused by a reduced number of insulin receptors on cells, or reduced effectiveness in binding to these receptors. The cause is complex and may involve genetic make-up, changes in lifestyle, nutritional habits, and environmental factors. 

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