Reduce IR and Save Beta Cells

Insulin resistance, inadequate insulin secretion, hormonal imbalances, stress and mitochondrial dysfunction play an important role in the pathogenesis of all form of Diabetes. Insulin Resistance results from inherited and acquired influences.
Hereditary causes of Insulin Resistance include mutations of insulin receptor, glucose transporter, and signaling proteins, although the common forms are largely unidentified.
Acquired causes of Insulin Resistance include physical inactivity, diet, medications, hyperglycemia (glucose toxicity), increased free fatty acids, and the aging process.
A sedentary lifestyle or lack of exercise reduces the function of insulin receptors present on the surface of each cell. This results in reduced muscular and tissue uptake of glucose and causes hyperglycemia. Insulin resistance results in increased insulin secretion to maintain normal glucose and lipid homeostasis. This compensatory hyperinsulinemia leads to endothelial dysfunction, atherosclerosis, metabolic syndrome, type 2 diabetes and cardiovascular diseases; in addition to Beta cell failure.

Classification of pre-receptor, receptor, and post-receptor causes of Insulin Resistance

(Source: Ref 34, Medscape – Insulin Resistance Sep 18, 2017. Author: Samuel T Olatunbosun)
Pre-receptor causes of insulin resistance include the following:

  • Abnormal insulin (mutations)
  • Anti-insulin antibodies

Receptor causes include the following:

  • Decreased number of receptors (mainly, failure to activate tyrosine kinase)
  • Reduced binding of insulin
  • Insulin receptor mutations
  • Insulin receptor–blocking antibodies

Post-receptor causes include the following:

  • Defective signal transduction
  • Mutations of GLUT4 

Mitochondrial dysfunction may play an important role in the development of insulin resistance and associated complications. Obesity, the most common cause of insulin resistance, is associated with a decreased number of receptors and with post-receptor failure to activate tyrosine kinase. Insulin binds and acts mainly through the insulin receptor and also acts via the insulin like growth factor–1 (IGF-1) receptor; cellular actions of insulin involve a wide variety of effects on post-receptor signaling pathways within target cells.

Specific causes of insulin resistance

  • Physical inactivity
  • Aging may cause insulin resistance through a decreased production of GLUT-4.
  • Increased production of insulin antagonists.
  • Glucocorticoid therapy is a common cause of glucose intolerance; impairment of glucose tolerance may occur even at low doses when administered for long term periods.
  • High sodium intake.

Increased levels of the acute-phase inflammatory marker C-reactive protein (CRP) are related to insulin resistance and the metabolic syndrome, suggesting a role for chronic low-grade inflammation. Dietary and endogenous Advanced Glycation End Products (AGEs) trigger a cascade of inflammatory mediators and cytokines like TNF alpha, NF kappa B, Interleukin-6 and Interleukin 1Beta; resulting in long term chronic low grade inflammation.
In skeletal muscle, various abnormalities, including defective glucose transport, may cause insulin resistance. Glucose transporter 4 (GLUT-4) is the main insulin-responsive transporter. Deficiencies of minerals like Chromium, Magnesium and Zinc may also contribute to the Insulin Resistance

How to reduce Insulin Resistance?

Exercise is the best way to reduce Insulin Resistance or improve Insulin Sensitivity. Regular exercise involving all major muscle groups in the body increases the number and function of Insulin Receptors. This helps muscular glucose uptake or insulin-mediated glucose uptake. Walking, running, swimming and outdoor sports activities can significantly reduce Insulin Resistance. A healthy diet should include nuts, fresh fruits, sprouts and vegetables (preferably raw). Avoidance of fried foods, roasted foods as well as foods cooked at high temperatures may be important to reduce the levels of AGEs (Advanced Glycation End products), ALEs (Advanced Lipoxidation End products) and AOPP (Advanced Oxidation Protein Products). AGEs, ALEs and AOPPs trigger chronic low grade inflammation, which is a major component of Diabetes and many other chronic diseases.
Some of the natural products mentioned earlier, for saving Beta Cells act by improving insulin receptor sensitivity, intracellular glucose transport (GLUT 4) and insulin signaling; thereby reducing Insulin Resistance. The natural products include Resveratrol, Pterocarpus and Curcumin which also play a major role in inhibiting ‘chronic low grade inflammation’.
Resveratrol significantly reduces Insulin Resistance [35, 36, 37]

Two meta-analyses of total 20 randomized controlled trials also confirm that Resveratrol significantly reduces insulin resistance and fasting plasma glucose [36, 37].

Salacia improves insulin resistance, glucose metabolism and reduces obesity [38].

Pterocarpus improves Insulin receptor sensitivity and induces PPAR alpha [8].

Gymnema augments glucose uptake and ameliorates insulin resistance by upregulating GLUT-4 (glucose transporter-4), peroxisome proliferator-activated receptor-gamma (PPAR gamma), adiponectin, and leptin levels [40].

Curcumin increases glucose uptake into skeletal muscle by improving the expressions of GLUT4 and reduces insulin resistance in muscular tissue through other mechanisms [30].

As mentioned earlier, the above natural ingredients (in Cresvin Beta) have significant anti inflammatory actions. In combination they have a synergistic action in reducing insulin resistance and thereby saving the Beta Cells. This could go a long way in reducing the morbidity of Diabetes and various life style diseases.

The Prevention and Remission of Diabetes – PROD Initiative is a holistic approach, laying greater emphasis on improvement of beta cell mass and function; through diet, exercises and reduction of mental stress, in addition to medication as advised by the Physician.

Please go to the Reference Articles.

Disclaimer: Cresvin Beta Team has taken maximum care to ensure that information is authentic. The information has been extracted from published medical trials and text books. The information is not meant to substitute a Physicians advice, nor is it meant to treat any disease. Members are advised to consult a Physician, Dietician, Physiotherapist or Trainer before taking medication or commencing an exercise program.