A great way to cure Diabetes through your diet!!!!!!

Here is an extremely amazing, healthy, safe and foremost natural way to cure the deadly syndrome DIABETES TYPE 2 .By a detailed study of previous article that is the "role of Adiponectin and Leptin in diminishing Insulin Resistance" I have revised a method of equipping few food substances which have the capability of sensitizing both Adiponectin and Leptin to a good extent when included in diet.

And the wonderful diet when followed regularly which will take you one step ahead to lead a healthy life without diabetes is here.

Before that please check your ORAL GLUCOSE TOLERANCE TEST:

follow these steps:

A standard dose of glucose which is 75grams  is ingested by mouth  and the blood sugar levels(mg/dL)                       should be checked  after 2 hrs. This test is to be performed morning and the glucose is to be drunk within 5 minutes.

Normal values for a 75g -oral glucose tolerance test for TYPE 2 DIABETES are:

fasting: 60-100 mg/dL

1hour :less than 200mg/dL

2hour:less than 140 mg/dL

If the value you received are  between 140-200 mg/dL

then you have impaired adipocyte differentiation

If the value you received are above 200 mg/dL the you have a 

higher sign of diabetes

After that follow this as your morning diet(breakfast):

 1)Robusta cofee,without much roasting, without milk(better if preffered)-207ml-gives you required (70mg    to 350 mg) of chlorogenic acid.

 2)Navy beans-1/2 cup (cooked)-gives you around 9.8g of amylose resistant starch

 3) Barley (ground)-100g  in 300ml of drinking water-gives you 4.3 to 5.5g of beta-glucans.

 4)Flax seeds(ground) -1 tablespoon (can be incorporated in diet anyway possible)-gives you 1.6g omega-3 fatty acid and 

5)Grapes-75g -gives you required amount of osmotin (which is said to mimic the role of adiponectin).

6)Eating wheat breads also would give you a considerable amounts of beta-glucans.

After having the above diet follow  these steps:

check  your blood sugar levels for 10min,15min,30min,60min and 120 min after this and note them down. I'm sure you do find some difference in the former and the latter values!!!

There you go, you have made a step ahead in leading  a healthy life. Follow this regularly for better results.

I request you to write about this diet you have followed and all the values before and after having the diet.

contact me in:  vaishnavinulureddi@gmail.com

post comments on how you feel about this.

Sources cited;

Very few considerably safe Drugs for Diabetes due to side-effects

When someone with type 2 diabetes needs a third medication to control blood sugar levels, the choice may come down to which drug has the least undesirable side effects, because the available medications all lower blood sugar in a similar manner.

That's the conclusion of a new review of data that shows there were no great differences in the ability of various classes of medication to lower blood sugar among type 2 diabetics, when used as "third-line" treatment (after a first and second drug don't suffice).

However, the study also found that some medications could cause weight gain, and some caused episodes of low blood sugar levels (hypoglycemia).
In any event, "type 2 diabetes is a progressive disease and most patients will need the combination of two or three anti-hyperglycemic agents to reach good glucose control in the long-term," noted the study's lead author, Dr. Jorge Gross, a professor of medicine at the Hospital de Clinicas de Porto Alegre, Brazil.

"The choice of the third agent should be individualized according to the characteristics of the patients and the undesirable effects of the medications, so you can't elect one agent to be used in all patients with type 2 diabetes," he explained.

The study results were published in this week's issue of the Annals of Internal Medicine.
Metformin, an older medication that's available as a generic, is generally recommended as a first-line treatment for type 2 diabetes, along with physical activity and diet changes. If metformin and lifestyle changes fail to control blood sugar well, a second drug is generally added.

For this study, the researchers chose the commonly used combination of metformin and a sulfonylurea. Drugs in the sulfonylurea class are usually available as generics and include: glyburide, glipizide, chlorpropamide, tolbutamide and tolazamide.
"This study looked at what's probably the most common combination of diabetes medications, but even the second-line therapy should be individualized based on the patient's needs," said Dr. Robert Henry, president of medicine and science for the American Diabetes Association.

Third-line medications in the current study included alpha-glucosidase inhibitors (acarbose), thiazolidinediones (which include Avandia and Actos), glucagon-like peptide-1 (GLP-1) agonists, and dipeptidyl peptidase-4 (DPP-4) inhibitors.
The review included 18 clinical trials with a total of more than 4,500 people. The studies lasted an average of more than 31 weeks.

When the researchers compared reductions in hemoglobin A1C (HbA1C) levels, they found no statistically significant differences between the third-line medications. HbA1C is a blood test that measures long-term (about two to three months) blood sugar levels.
Weight gain was more common in people taking insulin or a thiazolidinedione. The average weight gain for those on insulin was about six pounds, according to the study. For those on thiazolidinediones, the average weight gain was more than nine pounds.

An average weight loss of 3.6 pounds was seen in people taking GLP-1 agonists, reported the study. Insulin was most likely to reduce blood sugar levels too much, raising the odds for hypoglycemia, according to the study.
Dr. Joel Zonszein, director of the clinical diabetes center at Montefiore Medical Center in New York City, stressed, however, that "these are mostly drug company studies, and they're not long-term studies."

This review "shows that giving a third agent can help, and it also shows us that these medications have both good and bad effects," he said. "But we really need long-term studies on combinations that aren't sponsored by the pharmaceutical companies."
The bottom line, according to Zonszein: "Each patient should be treated individually. Are they obese? If yes, there are certain medications like insulin and thiazolidinediones that may cause weight gain we don't want."

When it comes to third-line agents, Henry said, another factor may be price. Some medications aren't always available in generic form, which may make them significantly more expensive.
If you have specific concerns, such as weight gain or cost, Henry said it's important to bring these concerns to your doctor's attention when you're talking about adding another diabetes medication.

"If a third medication is needed because glucose control isn't adequate, get one that's tailored to your unique needs," he advised.
"We think that the results of this study offer a wide range of choices of anti-hyperglycemic agents that might be used as the third option in patients with type 2 diabetes not controlled using metformin and sulphonylurea based on efficacy. The final decision would depend on the effects in weight and risk of hypoglycemic episodes," said Gross.

Info from- US NEWS health

The Role of Adiponectin and Leptin in diminishing Insulin Resistance

Introduction

‘A family history, a chemical mystery or a diet and an exercise chemistry’- anything may today

 bring a person down from being healthy. And Diabetes Mellitus is the most common one, more commonly T2DM which is letting millions of people down either due to their sedentary lifestyle or inheritance. Globally, as of 2010, an estimated 285 million people have type 2 diabetes, making up about 90% of the total diabetic cases. There are several deleterious  complications that 

made me throw the spotlight over this aspect like diabetic ketoacidosis, retinopathy, neuropathy, atheroschlerosis, etc.

On reference to many clinical evidences and research papers, obesity happens to be one of the

 most important contributor to the increase in the insulin resistance as well as type 2 diabetes.

 This means insulin resistance is associated with accumulation of body fat like skeletal muscle

 lipid over supply, etc.

ADIPONECTIN

Adiponectin is a protein hormone that modulates a number of metabolic processes, including 

glucose regulation and fatty acid catabolism. Adiponectin is exclusively secreted from adipose

 tissue into the bloodstream and is very abundant in plasma relative to many hormones. Levels

 of the hormone are inversely correlated with body fat percentage in adults .Transgenic mice with increased adiponectin show impaired adipocyte differentiation and increased energy

 expenditure associated with protein uncoupling.  Adiponectin is secreted into the bloodstream

 where it accounts for approximately 0.01% of all plasma protein at around 5-10 μg/mL. Levels of 

adiponectin are reduced in diabetics compared to non-diabetics. Weight reduction significantly increases circulating levels.

Adiponectin automatically self-associates into larger structures. Initially, three adiponectin

 molecules bind together to form a homotrimer. The trimers continue to self-associate and form hexamers or dodecamers.

 Role of Adiponectin in AMPK activation  
 Adiponectin is a protein hormone that has positive metabolic effects like enhancing fatty-acid oxidation and glucose utilization in muscle and adipose tissue as well as in inhibiting gluconeogenesis  in liver where these are associated with the activation of AMPK(1,4) in muscle and liver and the activation of the nuclear factor-kb in muscle cells. Hexameric and HMW forms activate NF-kb in undifferentiated and differentiated c2c12 cells and improve insulin sensitivity in liver whereas trimeric forms activate AMPK in muscle and adipose tissues. (Muscle cells trimeric adiponectin causes a rapid 2-fold increase in 5’-AMP level)AMPK when activated by adiponectin phosphorylates  and inactivates acyl-coA Carboxylase (ACC) which is the enzyme that catalyzes the formation of Malonyl-CoA. Malonyl-CoA is a substrate for the fatty-acid bio-synthesis and inhibits fatty-acid oxidation. AMPK activation by adiponectin results in inhibition of fatty-acids and triglyceride synthesis and stimulation of FA beta-oxidation.

AMPK phosphorylates IRS-1 at ser789 which correlates with a 65% increase in insulin stimulated pl3k activity in c2c12 myotubes, since AMPK activates aPKC which plays a positive role in glucose transport. Adiponectin also increases PPAR-Y ligand activity.

   
Adiponectin and acyl-coA synthase

 Acyl-CoA synthetases catalyze the 1^st step of fatty acid metabolism;

  FA + CoA + ATP ͢Fatty acyl CoA + 5’ AMP +2 Pi and the activation of FFA’s to their CoA derivatives by these enzymes generate 5’ AMP. The resultant formed during the attachment  of FA’s  to CoA would then activate AMPK.( The result is ATP consumption and  AMP production)

LEPTIN

Leptin  is an adipose derived  protein hormone that plays a key role in regulating energy intake and energy expenditure, including appetite and metabolism. It promotes appetite suppressants  like α-MSH and lowers the hunger. Leptin acts directly on the cells of the liver and skeletal muscle where it stimulates the oxidation of fatty acids in the mitochondria. This reduces the storage of fat in those tissues (but not in adipose tissue). The absence of leptin leads to uncontrolled food intake and results in obesity. The obese people have high levels of leptin and consequently result in leptin desensitization. In a report, baseline plasma leptin did not significantly differ between subjects with newly diagnosed or long-standing type 2 diabetes compared with non diabetic controls matched for BMI; however, plasma leptin responsiveness to dexamethasone was impaired in the diabetic groups. Leptin may improve glucose uptake by muscle and decrease hepatic glucose production . Finally, there is evidence that leptin may protect against the adverse effects of fat accumulation within non adipose cells. Less circulating leptin may lead to improved sensitivity to leptin, possibly offsetting the consequences of the reduction.

Role of leptin in AMPK activation
  Leptin  stimulates phosphorylation and activation of the alpha2 catalytic subunit of AMPK           (alpha2 AMPK) in skeletal muscle, thus establishing signalling pathway for leptin. Early activation of AMPK occurs by leptin acting directly on muscle, whereas later activation depends on leptin functioning through the hypothalamic-sympathetic nervous system axis. In parallel with its activation of AMPK, leptin suppresses the activity of ACC, thereby stimulating the oxidation of fatty acids in muscle. AMPK activation inhibits the phosphorylation of ACC stimulated by leptin. We can identify AMPK as a principal mediator of the effects of leptin on fatty-acid metabolism in muscle

COMBINATION OF ADIPONECTIN AND LEPTIN

Through analysis of multi-variated research studies it can be suggested that the combination of

 leptin and adiponectin at the molecular level would completely reverse the insulin resistance syndrome. Other studies have shown that insulin resistance in lip atrophic mice can be effectively reversed by the combination of physiologic doses of adiponectin and leptin, but only partially by

 either alone.

HYPOTHESIS

It has been hypothesised that combination of both adiponectin and leptin would lead to a rapid increase in the AMPK activity rather alone and combining these would double the positive effects in reducing Insulin Resistance. They may suppress the ACC activity at a better potential.

The combination of  the  aspects that lead to insulin sensitivity and addition of these to the

 existing drugs for IR may improve the medication and help many people get away from this

 deadly metabolic syndrome or  may also give rise to a completely new drug to treat T2DM and

 IR. It would also more effectively help in reducing the wide-spread obesity and prevent its further complications.

REFERENCES

       Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise

       Michael P Corcoran,Stefania Lamon-Fava, and Roger A Fielding

       Intramyocellular lipid kinetics and insulin resistance     ZengKui Guo

       Novel role of FATP1 in mitochondrial fatty acid oxidation in skeletal muscle cells   David Sebastián*§,  Maria Guitart§**, 

         Contraction of insulin-resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolismJohn P. Thyfault1, Melanie G. Cree2, Donghai Zheng3

       Adiponectin and Leptin in Relation to Insulin Sensitivity

GEETHA R. SOODINI, M.D., and OSAMA HAMDY, M.D., Ph.D.

    www.resistantstarch.com/NR/rdonlyres/

    A Potent and Selective AMPK Activator That Inhibits de Novo Lipogenesis

    Efficacy of Metreleptin in Obese Patients With Type 2 Diabetes: Cellular and Molecular Pathways Underlying Leptin Tolerance

-Vaishnavi.NR