Trained by JP - Insure GDA

€ 44,95

In-Sure is a unique glucose partitioning agent combining a potent blend of insulin sensitizing, glucose disposal and insulinomimetic agents to support healthy glucose metabolism and pancreatic beta cell function (60 servings/180 caps)

Per Serving (3 capsules):

  • 1000mg Berberine (from HCl 97%)
  • 500mg Bitter Melon
  • 350mg Benfotiamine
  • 300mg Alpha Lipoic Acid
  • 25mg Vanadyl Sulphate (20%)
  • 2mg Black Pepper Extract
  • 500mcg Chromium Picolinate

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Trained by JP - Insure GDA

€ 44,95

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Description
Type 1 diabetes is an early-onset autoimmune disease that leads to destruction of insulin-secreting pancreatic βeta cells; while type 2 diabetes shows insulin resistance in liver, muscle and adipose tissue, eventually leading to βeta cell failure in later stages.
Insulin resistance is defined as an impaired response of the body to insulin. The progression of type 2 diabetes, which starts with insulin resistance, is mainly driven by genetic and environmental factors (diet/supplements). When this occurs, initial problems with insulin action may be compensated by increased insulin secretion (hyperinsulinaemia) to maintain normal blood glucose regulation. Type 2 Diabetes occurs when the secretory function of β-cells cannot compensate for the further decreased insulin sensitivity; resulting in ultimately lower insulin production and higher blood glucose concentrations and possible -cell death.
In the liver, insulin resistance is characterised by excessive glucose production (gluconeogenesis) in the fasting state (high fasting blood glucose) and reduced glucose uptake after a meal, regardless of the presence of insulin, resulting in skewed triglyceride metabolism. In muscle, insulin resistance shows impaired glucose uptake, all leading to postprandial hyperglycaemia (elevated blood glucose), possible arterial inflammation and poor nutrient release/recovery.
In enhanced bodybuilding, GH and exogenous insulin are two compounds used for a wide range of benefits and potential applications. In both healthy subjects and people with type 1 diabetes, GH increases fasting glucose production through hepatic gluconeogenesis and glycogenolysis, and reduces peripheral glucose utilisation through inhibition of glycogen synthesis and glucose oxidation; leading to an increase in fasting blood glucose levels.
Berberine is the main active ingredient of an ancient Chinese herb Coptis chinensis French, which has reportedly been used to treat diabetes for thousands of years, with berberine hydrochloride being the most popular form of berberine used in studies. In one study, 500 mg of berberine three times daily was comparable to metformin in terms of hypoglycaemic effect, resulting in a significant decrease in haemoglobin A1c (HbA1c; from 9.5% ± 0.5% to 7.5% ± 0.4%, P<0.01), fasting blood glucose ( FBG: from 10.6 ± 0.9 mmol/L to 6.9 ± 0.5 mmol/L, P<0.01), postprandial blood glucose (PBG; from 19.8 ± 1.7 to 11.1 ± 0.9 mmol/L, P<0.01).
The mechanism of berberine on glucose metabolism has never been exclusively elucidated. Through activation of adenosine monophosphate kinase (AMPK), berberine can stimulate glucose uptake in muscle, liver and adipose tissue and inhibit gluconeogenesis in the liver through down-regulation of gluconeogenic enzymes. Berberine can also exert an anti-inflammatory effect on adipose tissue induced by a high-fat diet via activation of AMPK, and it has also been shown to down-regulate the expression of genes involved in lipogenesis and up-regulate those involved in energy consumption in adipose tissue and in muscle.
As an aside, insulin increases cellular glucose uptake by promoting GLUT4 expression on the cell surface through the activation of phosphatidylinositol 3-kinase (PI3K), while berberine increases glucose transport by enhancing GLUT1 gene expression independently of GLUT4. Berberine also has profound effects on insulin sensitivity by increasing insulin receptor (InsR) expression in a dose- and time-dependent manner; enhancing cellular glucose consumption in the presence of insulin and has the potential to modulate the gut microbiota in favour of lowering lipopolysaccharide (LPS) from unfavourable bacteria and reducing glucose transport through the intestinal endothelium, which in some people may contribute to the adverse gastrointestinal effects of berberine .
Hyperglycaemia along with the increased availability of free fatty acids; a consequence of deregulated lipolysis in adipose tissue are the two dominant metabolic changes that characterise glucotoxicity and lipotoxicity in diabetes involved in the development of vascular complications. Berberine can also counteract such various adverse effects of hyperglycaemia on the endothelium of blood vessels, including the inhibition of high glucose-induced reactive species, cellular apoptosis and inflammation that can lead to damage and potential for atherosclerosis. Berberine has also been shown to increase the excretion of cholesterol from the liver into the bile and eliminated through the faeces, thereby lowering serum cholesterol and triglycerides. Poor absorption in the small intestine is a key factor currently limiting the efficacy of BBR, as 80% of berberine is metabolised in the liver and intestine by CYP2D6. To improve efficacy, it is therefore necessary to improve bioavailability, which can be done by enhancing intestinal permeation through the addition of a "bio-enhancer" such as bioperine.
Benfotiamine, a lipophilic derivative of thiamine, has been proposed as a new therapy for diabetic complications. Benfotiamine is converted into thiamine pyrophosphate, a cofactor of transketolase; a coenzyme that plays a fundamental role in intracellular glucose metabolism. Activation of transketolase plays a crucial role in oxidative and non-oxidative pentose phosphate pathways that inhibit vascular complications of diabetes. Doses ranging from 150, 320 and even 1000 mg are well tolerated in the literature.
Benfotiamine blocks destructive biochemical pathways by which high blood sugar levels can damage nerves and small blood vessels, and also inhibits the formation of advanced glycation end products (AGEs) in both diabetic and normally ageing organisms. The most prominent marker of glycation in healthy subjects is haemoglobin A1c (HbA1c).
Besides its detrimental effects on the vascular system, hyperglycaemia can also contribute to insulin resistance in skeletal muscle, and it has been shown that myotubes (muscle cells) exposed to chronic hyperglycaemia show increased lipogenesis and intramyocellular triacylglycerol (IMTG) accumulation (increased fat deposits within muscle cells). The mechanisms by which these effects occur are complex and remain unknown, but may involve mitochondrial dysfunction.
Oral benfotiamine results in a 10-40% increased uptake of thiamine in liver and heart, while uptake is 5-25 times higher in muscle and brain tissue. One study showed that benfotiamine, but not thiamine, causes a marked increase in mitochondrial glucose oxidation in human skeletal muscle cells by also reducing NADPH oxidase 4 (NOX4) gene expression and preventing vascular damage. The marked down-regulation of NOX4 was observed in response to benfotiamine. NOX4 is upregulated in response to hyperglycaemia and is a primary source of reactive oxygen species that can cause vascular damage.
Alpha-lipoic acid is a biological antioxidant and natural cofactor of mitochondrial dehydrogenase complexes that is considered safe and well tolerated in the treatment of diabetic neuropathies. Alpha-lipoic acid (ALA) is synthesised by the liver and exists as two different enantiomers: the biologically active (R) isomer and the (S) isomer. ALA is normally commercially available as a racemic mixture (50:50) of the two. In vitro studies have shown that R-ALA can specifically activate two key molecules of the insulin signalling pathway - insulin receptor substrate-1 protein (IRS-1) and PI3K, resulting in an increase in glucose uptake via the glucose transport system in skeletal muscle and adipocytes resulting in the potential to mimic insulin action via the insulin signalling pathway. ALA has also been shown to improve insulin sensitivity in skeletal muscle cell cultures and increase insulin sensitivity in animal models of type 2 diabetes and insulin resistance. ALA significantly improves glucose transport activity, as well as both oxidative and non-oxidative pathways of glucose metabolism. In one study after 4 weeks of treatment with 600 mg ALA, insulin sensitivity in terms of glucose elimination rate was impressively increased and there was no significant difference between diabetics and controls with a fasting plasma glucose reduction of 6.47 ± 1.13 before treatment to 5.92 ± 0.83 mmol/l after treatment.
Vanadyl sulphate (VOSO4) is an oxidative form of vanadium, which has been shown to reduce hyperglycaemia and insulin resistance in vitro and in animal models of diabetes. In vitro, vanadium stimulates glucose uptake and oxidation, and glycogen synthesis in skeletal muscle; improving glucose tolerance without increasing plasma insulin. Vanadium compounds have also been found to exhibit insulin-like activity by mimicking insulin actions via insulin receptor tyrosine kinase activation and kinase phosphorylation cascade pathways.
It is thought that the action of vanadium may be to enhance the action of insulin on lipolysis and endogenous glucose production (EGP). The glucose-lowering effect of VOSO4 correlates well with a reduction in EGP but not with insulin-mediated glucose disposal, suggesting that the liver rather than muscle is the primary target of VOSO4 action at therapeutic doses for type 2 diabetes.
The metabolic effects of vanadium are known to be dose-dependent and require more than 4 weeks for a complete response. In one study, poorly controlled patients with type 2 diabetes were treated with 150 mg/day VOSO4 for 6 weeks and glucose tolerance, and liver/muscle tissue sensitivity was quantified. The results showed in type 2 diabetes that a key mechanism of action of VOSO4 is to decrease basal EGP, which mainly reflects glucose produced by the liver. The decrease in HGP correlates closely with the decrease in fasting plasma glucose (FPG). Corresponds to previous results. During an oral glucose tolerance test, plasma insulin levels did not change, confirming the results of animal and human studies that VOSO4 does not stimulate insulin secretion. However, the mechanism(s) by which VOSO4 reduces glucose output by the liver remains to be fully determined, but in type-2 diabetic patients, it is appreciated to improve glycaemic control by reducing basal endogenous glucose production and increasing insulin sensitivity of skeletal muscle.
Chromium is an essential mineral that appears to play a beneficial role in the regulation of insulin activity and its effects on carbohydrate, protein and lipid metabolism. Chromium is an important factor in improving insulin activity and helping glucose tolerance. Chromium has shown beneficial effects in improving insulin resistance in some clinical trials, but not in others. The two most common forms of chromium are the trivalent (3+) and hexavalent (6+) forms. Chromium 6+ does not occur in nature and is toxic. The chromium found in food and dietary supplements is the trivalent form. The role of trivalent chromium in glucose metabolism has been known since the 1950s. Chromium can alter insulin sensitivity at the cellular level. Although chromium's role as a cofactor for insulin action is not fully understood, it is considered a component of glucose tolerance factor; a complex containing both chromium and niacin that may be required for normal glucose tolerance. Glucose tolerance factor (GTF) is thought to be synthesised in vivo from absorbed dietary chromium, and acts as a physiological enhancer of insulin activity, binding to insulin and enhancing its action approximately threefold.
However, there is no reliable method to assess the chromium status of the body and there is no information on the bioavailability of the different forms of chromium. The metabolism of chromium is also affected by several factors, including stress, diet, exercise, diabetes and increased intake of simple sugars; all of which result in increased chromium loss. Studies show that people with type 2 diabetes have lower blood chromium levels than those without the disease. The ability to convert chromium into a more usable form may be the main difference between chromium metabolism in diabetics compared to non-diabetics. Patients with diabetes have been shown to have higher chromium absorption but also greater chromium excretion. The metabolism of C-Reactive Protein (CRP, a marker of inflammation) and insulin also seems to be regulated by plasma levels of chromium. When chromium levels are significantly lower (as observed in diabetics), insulin is up-regulated; while when plasma levels of chromium are significantly higher (normal healthy population), insulin and CRP levels are down-regulated. The mechanisms by which chromium metabolism affects plasma insulin and CRP levels are unclear, but may be related to chromium's beneficial effect on insulin sensitivity.
Specifically, chromium picolinate is the most effective form of chromium supplementation that has been shown to reduce insulin resistance and help reduce the risk of cardiovascular disease and type 2 diabetes. Note that dietary chromium is poorly absorbed; levels decrease with age, and supplements containing 200-1,000 mcg of chromium as chromium picolinate per day were found to improve blood glucose regulation. Numerous animal studies and human clinical trials have shown that chromium picolinate supplements are generally considered safe (GRAS). Because chromium enhances the action of insulin, chromium supplements can help lower blood sugar levels and improve glucose tolerance.
In this context, In-Sure has been formulated to use a standard dose of 500 mg berberine with the addition of 2 mg black pepper extract containing bioperine to improve intestinal absorption. 350 mg benfotiamine is included for its potential benefit in AGE prevention and HbA1c improvement and 250 mg alpha-lipoic acid to improve glucose oxidation and glucose removal. Finally, 25 mg vanadyl sulphate and 500 mcg chromium picolinate complete the ingredient profile to enhance and improve endogenous insulin sensitivity.
TrainedbyJP Nutrition has specifically formulated In-Sure as a potential compound solution to try to reduce some of the side effects in blood glucose metabolism that may arise as a result of the dietary choices/environment (high carbohydrate/high fat consumption) or supplementation (exogenous GH/insulin) involved in bodybuilding at highly competitive advanced levels.
Formulated together with Dr Dean St Mart.
Per serving 2 capsules:
  • 1000 mg berberine (from HCl 97%)
  • 350 mg benfotiamine
  • 500 mg bitter melon
  • 300 mg alpha-lipoic acid
  • 25 mg vanadyl sulphate (20%)
  • 2 mg black pepper extract
  • 500mcg chromium picolinate

References

  • Holt, R et al. Growth hormone, IGF-I and insulin and their abuse in sport. Br J Pharmacol. 2008. 154(3): 542-556.
  • Yin, J et al. Efficacy of Berberine in Patients with Type 2 Diabetes. Metabolism. 2008. 57(5): 712-717.
  • Affuso, F et al. Cardiovascular and metabolic effects of berberine. World J Cardiol. 2010. 26; 2(4): 71-77.
  • Lan, J et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. J Ethnopharmacol. 2015. 23;161:69-81.
  • Wang, Y et al. Update on the Benefits and Mechanisms of Action of the Bioactive Vegetal Alkaloid Berberine on Lipid Metabolism and Homeostasis. Cholesterol. 2018; 2018: 7173920.
  • Wang, H et al. Metformin and berberine, two versatile drugs in treatment of common metabolic diseases. Oncotarget. 2018. 9(11): 10135-10146.
  • Liu, D et al. Berberine Modulates Gut Microbiota and Reduces Insulin Resistance via the TLR4 Signaling Pathway. Exp Clin Endocrinol Diabetes. 2018. 126(8):513-520.
  • Beltramo, E et al. Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications. Acta Diabetologica. 2008. 45(3):131-41.
  • Alkhalaf, A et al. Effect of Benfotiamine on Advanced Glycation Endproducts and Markers of Endothelial Dysfunction and Inflammation in Diabetic Nephropathy. PLoS One. 2012. 7(7): e40427.
  • Fraiser, D. A et al. Benfotiamine increases glucose oxidation and downregulates NADPH oxidase 4 expression in cultured human myotubes exposed to both normal and high glucose concentrations. Genes Nutr. 2012. 7(3): 459-469.
    https://www.lifeextension.com/Magazine/2008/4/Protecting-Against-Glycation-High-Blood-Sugar-With-Benfotiamine/Page-01
  • Nicheva, A et al. Improvement of insulin sensitivity in patients with type 2 diabetes mellitus after oral administration of alpha-lipoic acid. HORMONES. 2006, 5(4):251-258.
  • Eason RC et al. Lipoic acid increases glucose uptake by skeletal muscles of obese-diabetic ob/ob mice. Diabetes Obes Metab. 2002. 4(1):29-35.
  • Ansar H et al. Effect of alpha-lipoic acid on blood glucose, insulin resistance and glutathione peroxidase of type 2 diabetic patients. Saudi Med J. 2011. 32(6):584-8.
  • Aharon, Y et al. Vanadyl Sulfate Does Not Enhance Insulin Action in Patients With Type 1 Diabetes. Diabetes Care. 1998. 21(12): 2194-2195.
  • Cusi, K et al. Vanadyl Sulfate Improves Hepatic and Muscle Insulin Sensitivity in Type 2 Diabetes. The Journal of Clinical Endocrinology & Metabolism. 2001. 86 (3): 1410-1417.
  • Missaoui, S er al. Vanadyl Sulfate Treatment Stimulates Proliferation and Regeneration of Beta Cells in Pancreatic Islets. J Diabetes Res. 2014. 2014: 540242.
  • Anon. A scientific review: the role of chromium in insulin resistance.Diabetes Educ. 2004. Suppl:2-14.
  • Sharma, S et al. Beneficial effect of chromium supplementation on glucose, HbA1C and lipid variables in individuals with newly onset type-2 diabetes. Journal of Trace Elements in Medicine and Biology. 2011. 25(3) : 149-153.
  • Hua, Y et al. Molecular Mechanisms of Chromium in Alleviating Insulin Resistance. J Nutr Biochem. 2012. 23(4): 313-319.
  • McCarty, M. The therapeutic potential of Glucose Tolerance Factor. Medical Hypotheses. 1980. 6 (11) : 1177-1189.
  • Ngala, R. A er al. The effects of plasma chromium on lipid profile, glucose metabolism and cardiovascular risk in type 2 diabetes mellitus. A case - control study. PLoS One. 2018; 13(7): e0197977.
Additional information
Number of servings per jar

60
Brand

Trained by JP