The biochemical properties of adipocytes have been clearly established in the medical literature. Depot-specific variances in said properties are involved in the development of diabetes, obesity, insulin-resistance, and weight gain.

Currently, type 2 diabetes is the most common metabolic disease in the world, afflicting more than 120 million people. Global scientific organizations have stated that by the year 2010, more than 220 million people are projected to have the disease by the year 2010 (1).

Insulin-related disorders, such as diabetes, obesity, and insulin resistance are causally related as each of those disorders are triggered by over-expression of blood glucose, insulin, LPL, and their subsequent shunting of foods into adipose tissue fat cell.

Peer reviewed, published studies have shown “A direct and causative relationship between the accumulation of intracellular fatty acid-derived metabolites and insulin resistance mediated via alterations in the insulin signaling pathway, independent of circulating adipocyte-derived hormones.”

As reported in 2005 Hypertension; 45:828, American Heart Association; Mechanisms of Insulin Resistance in Humans and Possible Links with Inflammation, “Although standard definitions of insulin resistance still define it in terms of the effects of insulin on glucose metabolism, the last decade has seen a shift from the traditional "glucocentric" view of diabetes to an increasingly acknowledged "lipocentric" viewpoint.

This shift to lipocentric relationships in insulin resistance has grown in popularity. As of 2007, scientists and research endocrinologists have embraced the strong connection between fat metabolism and insulin resistance.
Insulin resistance plays a primary role in the development of type 2 diabetes mellitus, and the mechanism by which insulin resistance occurs is related to alterations in fat metabolism (2).

Clinically defined, insulin resistance is “A state of reduced responsiveness to normal circulating levels of insulin, which plays a major role in the development of type 2 diabetes.”

It has been clearly demonstrated that insulin resistance is a major factor in the pathogenesis of diabetes, obesity and weight gain. Insulin resistance is biochemically tied to Leptin and Lipoprotein Lipase (LPL).

In humans, the primary mechanism for fat storage is Lipoprotein Lipase (LPL), known to scientists as the “Gatekeeper for fat-storage in the fat cell.”

Orally ingested agents, such as sugars, carbohydrates, and starches, either stimulate LPL or negate its potent fat-storage sequence.

Fat-derived circulating hormones include Leptin, LPL, adipsin, Acrp30/adipoQ (adipocyte complement-related protein of 30 kDa), and Resistin, all primary factors in causing whole-body insulin resistance related to obesity (3).

The accumulation of intracellular fatty acid-derived metabolites is triggered by a mechanism which causes tissue-specific increase in LPL resulting in tissue-specific insulin resistance.

Overexpression of Lipoprotein Lipase, in either liver or skeletal muscle, accumulates lipid (in corresponding tissue) and proceeds to manifest insulin resistance in a tissue-specific manner.

Fat-storage mechanisms in humans involve lipid accumulation due to enhanced fatty acid uptake into the muscle coupled with diminished mitochondrial lipid oxidation. Excess fatty acids are esterified and take one-of-two pathways; they are either stored or metabolized.

The storage versus metabolized routes to various molecules results in the interference with normal cellular signaling, particularly insulin-mediated signal transduction, thus altering cellular and, subsequently, whole-body glucose metabolism.

If not managed by dietary intervention, impaired insulin responsiveness can progress to type 2 diabetes mellitus. For the majority of the human population, this biochemical cascade is avoidable, given that causes of intramyocellular lipid deposition are predominantly diet and lifestyle-mediated.

Chronic overconsumption of foods and beverages that stimulate LPL have been shown to increase the risk of insulin resistance, leading to type 2 diabetes, insulin resistance, obesity, and weight gain.

Since LPL activity can be controlled by adjusting the consumption of LPL-activating foods and drinks, LPL’s profound adipose tissue fat-storing proclivities can be controlled by reducing/eliminating dietary exposure to LPL-stimulating agents.

All sweeteners, carbohydrates, sugars, starches, and other ingredients used in prepared foods and beverages, as well as any raw material, possess intrinsic biochemical characteristics that determine their role in adipose tissue physiology, including its LPL, insulinogenic, blood glucose, glycemic, adipocyte, and fat-storing properties.

Studies of glucose disposal in normal humans shows that skeletal muscle accounts for the majority of insulin-stimulated glucose uptake and that more than 80 percent of this glucose is then stored as glycogen. (Shulman GI et al. Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy. N Engl J Med. 1990; 322: 223–228)

The rate of glycogen synthesis in skeletal muscle is 50% lower in diabetic subjects than in normal volunteers. The only other organ capable of storing a significant amount of glycogen is the liver, and glycogen stores are reduced in diabetics.

This glycogen synthesis malfunction in type 2 diabetics is mediated by dietary ingestion of high glycemic foods and drinks, the majority of which contain LPL stimulating ingredients, such as sucrose, glucose, dextrose, maltodextrins, glucose polymers, and other high glycemic raw materials. All high glycemic foods, drinks, and raw materials over-elevate blood glucose levels, and negatively affect insulin and LPL.

In non-diabetics, dietary fat-storage mechanisms are intrinsically the same as in diabetics, yet the reaction in diabetics is profoundly more intense and has more serious implications in blood glucose and insulin imbalance.

Glycogen synthesis malfunction and vital muscle glycogen replenishment cannot be controlled by ingestion of high glycemic carbohydrates, sugars, and starches, which exacerbate insulin resistance, LPL stimulation, and fat-storage into fat cells. Persons with type 2 diabetes are, inevitably, overweight or obese; conditions caused by continual ingestion of high glycemic foods and drinks, as they cause LPL activation.

Artificial sweeteners that have -0- calories, and -0- carbohydrates do not replenish muscle glycogen, thus sports drinks with -0- calories and -0- carbohydrates are contraindicated in sports performance, as they can lead to “Hitting-the-Wall” syndrome, reduced performance, and/or hypoglycemia.

The human body, and particularly the brain, cannot function in a -0- carbohydrate environment. Yet essential carbohydrates, starches, sweeteners, and sugars used in all foods, beverages, and edibles typically elicit high glycemic, fat-storage properties, creating a biochemical cascade of reactive hypoglycemic, sweet-cravings, LPL stimulation, impaired sports performance, reduced cognitive function, and adipose tissue fat-storage.

In 1983, researchers began developing raw materials that do not possess the metabolic activities of high glycemic sugars, carbohydrates, and starches. In 1997, the process for extracting glycosides from natural fruits had evolved into a feasible and affordable alternative to raw materials that stimulate LPL, imbalance Leptin, are high glycemic, and that cause deposition of adipose tissue fat in humans (published United States Patent Office).

The researchers received the first glycemic patent ever awarded worldwide, and went on to develop and file patents on low glycemic carbohydrates, starches, and raw materials, utilizing a proprietary 32-step extraction process to remove the glycosides from fruits.

The natural glycoside fruit extracts (Trutina Dulcem) derived from this process do not stimulate LPL and have been Certified as “Low Glycemic.”

Following a 20 + year research project, including use of the glycoside Trutina Dulcem in over 250,000 people over a 15 year-period, the resulting Low Glycemic carbohydrates, sugars, and starches derived from Trutina Dulcem have been expanded to fulfill market demand for Low Glycemic raw materials.

Trutina Dulcem has undergone numerous Human In Vivo Clinical Trials and has proven to be an “Anti-Carbohydrate” (4) in diabetics and non-diabetics.

To ascertain the interaction between Trutina Dulcem and Lipoprotein Lipase and Leptin, Trutina Dulcem (TD) was analyzed to determine its “anti-carbohydrate” properties and to quantify the precise mechanism by which TD blocks adipose tissue fat-storage.

Ramis JM et al, Journal of Nutritional Biochemistry; 2005, demonstrated that “The Leptin content of fat depots as well as plasma insulin concentrations appear in our population as the main determinants of adipose tissue LPL activity, adjusted by gender, depot and BMI” and that “Tissue leptin and plasma insulin are associated with lipoprotein lipase activity in severely obese patients.”

To this end, depot-related and gender-related variances in LPL were examined in non-diabetic obese men and women. Endocrine and biometric factors were rated for their dependence on fat depot and gender. Activity and expression of Lipoprotein Lipase (LPL) were analyzed in adipose tissue fat samples from visceral and subcutaneous fat deposits.

The all-natural glycoside Trutina Dulcem, and its raw material components, TD Low Glycemic carbohydrates, sweeteners, sugars, and starches, are suitable for inclusion in weight management products, as well as all applications in Low Glycemic foods and beverages.

Unlike chemical and synthetic sweeteners, all-natural Trutina Dulcem (TD) is suitable for children and pregnant women. Additionally, TD does not exacerbate ADD or Dyslexia, and does not stimulate human fat-storing mechanisms.