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Diabetes Drug Development - Science topic

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is diabetes t2 curable? reversible ? than it means you are cured? or you are always a diabetic person? Thank you
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Diet is known to alter the gut microbiota. Is it likely that processed foods and high glycemic index foods may bring about such a change which in turn may lead to inflammatory and other changes progressing to diabetes?
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Dear All,
I am looking for papers or evidences for loss of insulin receptor in case of diabetes. I am interetsed to know more about insulin resistance development based on insulin receptor loss. Please give your comments on the same.
Thanks and reagrds,
Diptiman
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Is there any literature available showing GLP-1 concentrations in humans with Metabolic Syndrome?
Equally is there any data in human showing DPP-4 concentrations in humans with Metabolic Syndrome?
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Does Sugar Feed Cancer? Exploring the Sugar and Cancer Connection
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Because if consume too much, it can cause many diseases, such as diabetes which damages one person's health....
Here, people are talked to eat or drink less sugar- or fructose-added foods or drinks.
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The dissacharidases are sucrase, lactase and maltase.
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Thank you SIR. I found your Idea helpful.
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Hi Everyone I am looking for antibodies for ER pathways that works in INS-1 cells or any other cells. There are lots of paper out there but I want to know if anybody have tried these antibodies in INS-1 cells and that has worked perfectly. The antibodies I am interested are as follows:
spliced-XBP1. p-PERK, PERK, p-IRE1 alpha, Total-IRE1 alpha, ATF4, ATF6 active.
Any information will be highly appreciated. Thanks in advance.
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UPR/ER stress is activated through an orchestrated interplay of signaling molecules from all three arms of the UPR pathway i.e. IRE1, ATF6, and PERK. This is why, it is critical to analyze signaling players in the context of the mentioned fact. Novus' ER Stress / UPR Antibody Pack contains sample size vials of the top markers namely: GRP78/HSPA5, pSer724 IRE1 alpha, total IRE1 alpha, XBP1, ATF6, and CHOP/GADD153. For scientific technical answers to over 15 similar questions, I would suggest reviewing our UPR and ER Stress FAQs at https://www.novusbio.com/support/upr-and-er-stress-faqs
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Our research group is interested in isolating the principal component from the commercially available drugs (for example anti-fungal and anti-diabetics). Is there some particular way to remove fillers from them?
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To address both issues raised by James and Eric:
Crush the pills, add water. The fillers will generally expand and turn the aqueous solution into a gel-like mess. Add ethanol or methanol this will "dehydrate" the gel making it easier to filter out. You could repeat this process with the remaining solid to maximize recovery. Then dry down the aqueous/alcoholic solution and redissolve in the appropriate solvent. Bear in mind this will include anything in the pills that are soluble in water and/or alcohol so you may need to further purify the active component.
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I am performing anti-diabetic activity by Alloxan induced model STZ model and some other models?
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Hau Van Doan · I also have decided to use Alloxan model please if you are having some papers on it please send me on sandeepschn@gmail.com
Thanks
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Hi! I am looking for diabetes patients' data set right from symptoms, physical examination, lab investigations,family history and risk factors. Can anybody help me ? We are building the physician recommendation system and currently we are focusing on diabetes for the pilot application. We can't proceed further due to lack of data. I would really appreciate if you can share or help me directing where can I find the data that I need in order to proceed further. Please help.
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I am not sure can answer such general question in a useful manner. It would be helpful if you specified at least the aim, ie.what is your planned "physician recommendation system" to do, and share more details re. target groups (what physicians: GPs? diabetologists? Which diabetes type? What patients? pre-diagnosed, diagnosed? What geographies is it for?).
Without knowing the above, I can only suggest some general links:
You may want to search for diabetes national surveys and reports in the EU and USA.
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please, can somebody explain how to carry out molecular docking studies on bioactive compounds against diabetes and cancer?
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Dear Abdulfatal,
(1) First,  you should search the literature for the chemical structures of these  compounds.
(2) You should know the receptor or the enzyme's active site that these compounds are bound to.
(3) You should find the global minimum structures for those compounds using UUF followed by semi-empirical method such as AM1 and PM3.
(4) Then you run a docking of these compounds with their corresponding receptor or enzyme. There are many docking programs; such as Amber, Charm and etc.
These docking calculations give you a picture on the energy binding of the compound and the receptor. strong binding is characterized will low energy and vice versa. 
Hoping this will be helpful,
Rafik
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I am doing antidiabetic activity of plant derived compound in Sprague Dawley rats. After the alloxan treatment, I will administer my drug in particular concentration. After certain period of time, I will check the blood glucose in tail vein blood using glucometer. And also, after sacrificing all animals, I will have to estimate serum glucose concentration by the glucose oxidase method. What might be the difference between the estimation of glucose in whole blood using glucometer and estimation of glucose in isolated serum or plasma by using glucose oxidase methods? What is the normal range of both in rat samples? Will you please help me to clarify this my basic doubt? 
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Hi
Dr Ananya Mandal, MD wrote:
Blood Sugar Glucose Measurement
Imbalances of blood sugar are common among patients of diabetes mellitus. Diabetes indicates persistently high blood sugar that may cause damage to various organs like the kidney, heart, small arteries and the eyes (retina).
Diabetics are also prone to sudden drops in blood sugar called hypoglycaemia. To monitory these fluctuations blood sugar measurement is vital in diabetic individuals.
Some of the considerations in blood glucose measurement include:
Sample
Glucose can be measured in whole blood or serum (ie, plasma). Earlier blood glucose was measured in whole blood. Nowadays serum is extracted from blood and glucose is measured in the serum. Whole blood and serum blood glucose is often different. Red blood cells have higher concentration of protein than serum and serum has higher water content and more dissolved glucose than whole blood. To obtain blood glucose in serum from figures in whole blood, it is multiplied by 1.15.
Blood is collected from a vein (usually in the crook of the arm). The blood sample is collected into vacuum tubes. Blood sample needs to be collected from a different arm other than the one where there is the intravenous line to prevent confusion of the results with the intravenous fluids. After meals the levels in the veins are somewhat lower than capillary or arterial blood. The estimate is by about 10%.
The surrounding temperature before processing affects blood glucose level estimation. At refrigerator temperatures, glucose remains relatively stable for several hours in a blood sample. At room temperature (25 °C), a loss of 1 to 2% of total glucose per hour is seen in whole blood samples.
If the blood is allowed to clot the glucose in the sample gets metabolized by the blood cells unless the cells are separated. If there are higher numbers of red or white blood cells there is excessive glycolysis in the sample with substantial reduction of glucose level. This occurs if the sample is not processed immediately and leads to a faulty result.
To prevent such losses blood samples are collected in Fluoride tubes (ie, gray-top) since fluoride inhibits glycolysis. Red-top serum separator tubes can also be used for samples after being centrifuged isolating the serum from cells.
Timing of the test
Blood sugar is measured at various points of time to give an idea about the body’s blood glucose regulation system. The primary test is the fasting blood glucose. (FBG). This is measured after overnight fasting. Blood glucose normally is lowest early in the morning after 6 to 8 hours of fasting overnight.
Two hours post prandial blood glucose or PPG is the next common test. After a carbohydrate rich, full meal, two hours are allowed to elapse before blood is taken again for estimation of glucose. This test gives an estimation of glucose handling by the body.
Other tests include oral glucose tolerance test (OGTT) and intravenous glucose tolerance test (IVGTT) wherein a fixed amount of glucose is administered orally or intravenously respectively and repeated blood sugar tests are performed to check on the body’s glucose handling.
Another important test is the glycosylated haemoglobin (HbA1C). This test gives an idea about fluctuations of glucose in blood over a period of last three months.
Blood glucose can also be self-monitored by the patient using meters or hand help portable monitors. Blood glucose is co-ordinated with urine glucose test as well.
Methods of blood sugar measurement
The earlier method used to measure blood sugar is a chemical method that exploits the ''nonspecific reducing'' property of glucose in a reaction with an indicator substance that changes color when reduced. There are other blood compounds like urea that also have reducing properties, this technique may yield faulty results. The method currently in use, utilizes enzymes specific to glucose and is less likely to yield errors of this kind.For more plz read at following links.
Regards
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what is the best biological procedure proving the action mechanism of a drug on PPARgamma and sulfonylurea receptor as antidiabetic agents?
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We used a PPARgamma transactivation assay published in: Planta Medica 10/2010; 77(4):346-53. DOI:10.1055/s-0030-1250382. May be it is useful for you too.
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I need papers about the effect of the acute effect of metformin in rodents as well as the chronic effect. I need to know which doses they use and which rout.
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Please apply to the papers of Prof V.Anisimov from our Institute and to my own review
Metformin in obesity, cancer   and aging: addressing controversies Aging (Albany, NY), 2012 Vol.4(5)320-329 
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I am attaching here with the details related to Indo- European Call on Health-“Diagnostics and interventions in chronic non-communicable diseases”
Please go through it. If anyone / professor / researcher, interested, can make collaborative proposals.
Semi Conductors Nano structures
metal-insulator transitions
Hybrid magnetic-semiconductor structures & Bio-nanomaterials
I have some experience / research interests in above fields. semi-conductor / magnetic / super-paramagnetic materials are useful in making bio-sensors / diagnostics. .
Also, I am attaching here with my recent achievements in nanotech field for references. http://goo.gl/jAFeCV 
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Epigraph = Perspective AGRO technologies.
(Letter - a request is sent for review to the Company's management, review and influencing the future development on the implementation of emerging technologies.)
Good afternoon, dear and respectable company!
Perspective Agro Industry TEAM ! As basis of future undustries !
To you with a proposal Oleg V. Anokhin, Dr. Of Chemistry scientist from Ukraine. (CV attached)
My suggestion is invited to consider the proposal invented technological cycle of deep processing of natural "factories" type fiber crops. http://en.wikipedia.org/wiki/Fiber_crop
I invented the process algorithm which yields (get) new natural raw materials for food industry perspective, medicine, new active functional components for them. Link - generally receive much more variety of useful materials, but now on your sector of interest.
With the use of basic knowledge in the areas of: physical chemistry, colloid chemistry of polymers, physical mechanics, organic and inorganic chemistry, quantitative and qualitative analysis, and ... a lot more then = offers innovative technological solution.
To my letter - proposal attached my basic message that (mostly) reveals the essence and the prospect of the invention.
Now, about the benefits and key points on the way to implement such technology as a separate plant or mobile ("flying" shop) processing complex.
As can be seen from the accompanying article, the key point (as required) is the proximity of the use of technology at the time of harvest yields. The spectrum of the interests of my constituents technology is amorphous natural "factories", their liquid phase. In other words, if we have time to "grab" the required components from natural "plant" in the time of harvest ... or they become "wood" is already on the field.
Even if you are working with only one source of raw materials - hardly at all areas (regions) crop ripens at the same time. Maybe this fact and for the better?
Hence the conclusion - I have to look for a high-tech company in the field of nutrition and components to them (!) A company having its other (partner) company that understands the creation of units in the cleaning of crops. Type John Deere, CLAAS, or etc .. That's not all of the requirements. Since the important point is - the proximity to the time of harvest (or near) - that ...., It is desirable to me (us) to be familiar with the companies that develop road tractor with possibilities "pull, pull" big trailers. In our case, it may be part of our preparation plant or facility for receiving raw materials and primary processing. Like Volvo Truck type, Kenworth Truck or etc.
In conclusion, I should add that I propose solutions and technological methods are my personal property. My activity in the search for a suitable partner is connected with the fact that on the territory of my homeland there are many current problems, which do not give me the opportunity to realize proposed. I have no real financial opportunities to fix the complex patent and further implementation of the proposed ideas in the "metal". In addition, my homeland (yet) NO ready to implement such high-tech solutions, while agrarian country.
4/23/2015 Sincerely, Oleg V Anokhin
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What mg STZ should we use to induce diabetes in mice?
Must we use to solve STZ in Citrat buffer pH:4,5 or another best way?
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We seek an alternate way, because mice are dead. We used STZ 90 mg/kg/day on consecutive days in Citrate Buffer.(i.p use). Some of them were dead, some of them were not to be DM.
How about %0,9 sterile saline solution rather than citrate buffer?
What do you think our dosage (90 mg/kg/day)?
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I have a very controversial question. Is it possible that a compound increases chop in a dose dependent manner in parallel decreases all other markers for apoptosis such as Cleaved caspase-3, Parp and TXNIP. I have read couple of post indicating Chop not being the best marker for apoptosis but can chop be cytoprotective? Comments will be highly appreciated. Thanks
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CHOP is induced by a number of stress stimuli.  All of these stimuli lead to the activation of one of the 4 kinases that phosphorylate eIF2a, i.e., GCN2, PERK, PKR and HRI. Each kinase is activated in response to specific set of stress stimuli.  Activation of these kinases leads to phosphorylation of eIF2a, the induction of ATF4 transcription factor and ultimately the induction of CHOP. This pathway is called the integrated stress response (ISR). 
There are a number of reports suggesting that CHOP induction is essential for stress-induced apoptosis.  Furthermore, it is suggested that CHOP is responsible for the regulation of Bcl-2 family of proteins and that is the mechanism by which it induces cell death.  However, accumulating data  from the CHOP deficient cells has shown that the rate of stress-induced (ER stress in particular) cell death is not affected in these cells. This suggest that CHOP is not required nor is essential for stress-induced apoptosis.  However, overexpression of CHOP is toxic in several cell lines. Some of the recent papers suggest that CHOP indirectly induces cell death through regulation of ER redox status and also through the reversal of the translational block.  
So, although CHOP is induced by the ISR, it is by no means a marker of apoptosis. You should still stick with the classical markers of apoptosis and use 2-3 of these in your studies, e.g., caspase enzymatic activity (DEVDase activity), or caspase-3/PARP cleavage, annexin V staining, morphological assessment (microscopy) etc.
Please be aware that CHOP can be induced by oxidative stress and ROS.  Oxidants / ROS can cause rapid inactivation of the cysteine residue in the active site of caspases leading to their inactivation and targeting them for degradation.  So if your compound is inducing ROS, it may induce CHOP, inactivate caspases and induce necrosis/necroptosis. 
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I have read a number of previous original research (including some reviews) that analysed the association between metformin use and risk of lactic acidosis.
In almost all studies, the outcome has been zero. However, there are some few case-control studies (and case series) that showed the likely association. 
Is there anyone aware of conference abstracts/unpublished data regarding this aspect? Kindly share.
Cheers!
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 Metformin inhibits cell respiration which cause increasing demand for  Anaerobic respiration (increase Lactic acid ) but this occurs when high doses of metformin were used in human and rodents.
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Elderly patients may have reduced renal function induced by age associated changes ( measurable ) and possible other changes.  All these, before comorbid conditions and polypharmacy. Please share your experience and opinion regarding the use of Metphormin as treatment of Diabetes mellitus in old age ?
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According to litterature, metformin could theoretically be safe until 30 ml/mn clairance, so...
But take care of creatinine value in elderly (denutrition...)
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I would like to know if anybody has any experiences with diabetes prevention programs in Community Pharmacies, something like Findrisc or similar. I would be most grateful for any information you have.
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Look for the GLICEMIA Study in Germany from Prof. Kristina Leuner.
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What are the solvents used to dissolve the standard (Diazoxide, Glibenclamide, Sulphanylurea) drugs for insulin assay of Pancreatic beta cells of rat growing in RPMI media?
I am performing a standard insulin assay using the Mercodia insulin kit. The cells are being grown in 96 well plates at 50k cells per well. 
Please also let me know the concentration of these drugs in the standard assay and cell number used per plate.
If possible, please also send me a few good but simplified papers on insulin assays.
Thanks !
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DMSO works!
Tolbutamide at 100 uM works with INS1E cells
Endocrinology. 2004 Feb;145(2):667-78. Epub 2003 Oct 30.
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I tried to induce diabetes in hamsters with high cholesterol diet by STZ injection. I used a dose of 50mg/kg BW for 3 consecutive days at non-fasting status. My hamsters died in the following 2 weeks. The remaining were high in plasma lipids and glucose with very bad health condition. How can I improve my protocol and decrease the mortality? Thank you
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Actually it depend on what type of diabetes u want to develop. In my case i want to develop type 2 so i hv tried 40-45mg/kg bw of STZ. In my opinion and experience, 60mg/kg bw might cause greater effect towards the subjects (maybe it seems to develop late-onset of diabetes characteristics)
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The compounds are synthesized by interaction of 2 materials together. The resultant legends molecular weights were calculated from its structure. I need to examine whether it will act as anti-diabetic or not?
All I have is the molecular weight
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i would estimate LD50 according to OECD 425 guidelines (OECD 2000), using the AOT425StatPgm software to calculate LD50, (http://www.epa.gov/oppfead1/harmonization/), and than dose the animals with 10.0% of estimated LD50, based on the outcome higher or lower dosages (usually 10-fold or 100-fold lower) can be tested. OECD 425 refers to oral administration, but can be accordingly implemented for i.v. administration. 
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Protocol for water deprivation test in patients with Diabetes Insipidus
Different books have different protocols
Dose of Vasopressin varies from 5U to 1U/m2
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I give you our protocol
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I am planning work aimed at evaluating hypoglycemic effects of camel milk. Main aim is differentiating effect due to high insulin content (DM Type I) or other hypoglycemic effect (DM - Type II). The plan is to induce DM pharmaceutically and assess potential effects of camel milk consumption on plasma glucose levels.
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It seems that you are not interested in studying the effects of camel milk on the development of autoimmune type 1 diabetes, but rather on hyperglycemia. Therefore, you would not use multiple low-dose streptozotocin (STZ)-induced model of T1D, but high-dose STZ-induced T1D. You can use either mice or rats for induction of that T1D model. 
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I want to study mode of action of a medicine used in traditional system of healing and want to check its mode of action. I will be doing my studies on mice models but do not wish to study mode of action in vivo. can HeLa cells be used?
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thank you Tausif Alam. i wish to study both type one and two diabetes.
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What is exact dose of STZ to induce diabetic type 2 in rats?
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Doses given on the based of Type I or Type II induction
35 mg STZ with diet for Type II
50 mg STZ  (minimum 2 times 1st day and 3rd day) This is my personal experience as getting rats diabetic first stretch is bit tough so have to give 2nd time STZ.
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hello, I recently was trying to make type II diabetic rats model by i.p injection STZ (65mg/kg). But the rats was dying in 5 days even I tried to give little insulin(4 IU) everyday since day 3 to control the deteriorated rats (blood glucose > 25) . Am I missing some important issue during performing animal model and how to increase the survival rate? Could anybody give some advice on this?
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The dose is a bit high. Most people use 60 mg/kg or less to induce Type 1 diabetes. You really cannot induce true Type 2 diabetes in a rat model using STZ.
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The best diabetes type-2 target.
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Dear SushilKumar:
if you are not understading leave it or learn from others, the question is that
what is the best therauptic target, if any body is working in drug development area, easily they can understand.
Regards
Venkatesham
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I am working on a molecule that stimulates insulin secretion but does not increase calcium influx in cultured pancreatic beta cell (MIN6 cell).
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It is important to define what you mean by "calcium-independent". Calcium is somewhat fundamental to the secretory process (among many cellular processes), so very little in a cell will function properly in the complete absence of calcium. That said, there are numerous examples of pathways that can potentiate insulin release without changes in calcium levels in the beta-cell provided there is sufficient calcium for exocytosis to occur. I’ve listed a few references as examples of this below. Also, note that the endoplasmic reticulum is such a huge source and sink for calcium that it has the potential to significantly alter calcium levels in the cytosol, mitochondria and nucleus. We touch upon this in a review article on the role of calcium in cytokine action in beta-cells (JW Ramadan et al. Cell Calcium, 50:481-90, 2011). Good luck with your studies!
Calcium-independent potentiation of insulin release by cyclic AMP in single beta-cells. Ammälä C, Ashcroft FM, Rorsman P. Nature. 1993 May 27;363(6427):356-8.
Relative contribution of Ca2+-dependent and Ca2+-independent mechanisms to the regulation of insulin secretion by glucose. Sato Y, Nenquin M, Henquin JC. FEBS Lett. 1998 Jan 9;421(2):115-9.
Glucose-dependent increase in mitochondrial membrane potential, but not cytoplasmic calcium, correlates with insulin secretion in single islet cells. Heart E, Corkey RF, Wikstrom JD, Shirihai OS, Corkey BE. Am J Physiol Endocrinol Metab. 2006 Jan;290(1):E143-E148. Epub 2005 Sep 6. PMID: 16144817
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I wanted to know which is the standard protocol that is followed. Hence, I wanted to know which is the standard protocol that is followed.
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I am wondering what responses you got to your question
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I want to do some type 2 diabetes studies in vitro for some homeopathic product to know the potency of the drug.
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Hi, it depends on what aspect of diabetes is your target. Are you looking to see the insulin-sensitizing or insulin secretion potential of your product, or its effect on any related complication? you could simply use muscle, liver or adipose cell lines to test the effect of the product on glucose uptake in the presence or absence of insulin and so on. You could also use pancreatic cell line to test insulin release. We have worked on these and also other complications of diabetes like the polyol pathway by studying the effect of our product on aldose reductase activity. In addition, we also study the transcriptional changes induced by our products in genes related to glucose metabolism.
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Streptozotocin destroys completely the beta cells in islets of langerhans (Mitochondrial DNA damage) and my doubt is whether the drugs/herbs can rejuvenate the dead cells?
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Thanks to Dr Salah and Dr Tejas for their clarification
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Except
PPAR
Glut4, C/EBP
Carbohydrate digestive enzyme inhibition
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SGLT2 inhibitors now started approval from USFDA. Cangliflozin, and very soon Dapagliflozin will be in the market from boerhinger.
SGLT2 target is the latest one
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From DPP study we know that metformin is effective for prevention of diabetes. Major recommendations like ADA standard of care 2013 advise using metformin for high risk patients. Beside biguanides there are evidence that other classes of anti-diabetic medicine (Alpha-glucosidase inhibitors, and thiaolidinedionses) that are also effective for prevention of diabetes. Is there any recommendation for usage of these drugs for preventive measures?
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NIDDM is progessive disease. Some studies showed reversal of the "prediabetes" stage. The only way to reverse it is certain types of bariatric surgeries, although long term follow up is still pending.
Most important for diabetes is prevention of future complications; life style changes will help this and improve glycaemic control with the help of medications.
More to know in the future.
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On what bases I can select the plant against diabetes? Is there any strategy for selecting plants for specific diseases.
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@Devendra,
Please go through the available literature on traditional medicinal plants used in the management of diabetes. From that you can select the plant species on which the detailed scientific studied have not been carried out so far.
Secondly you look for the chemical compounds responsible for the antidiabetic activity of the plant species. You can select the species having these phytochemicals and study it for the same activity.
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Kindly suggest the moderate dose of STZ to induce diabetes in Rattus norvegicus for evaluating antidiabetic activity of herbal plants. We administered STZ with sodium citrate buffer (4.5 pH) with a dosage of 35 mg/kg body weight of rat through i.p at single dose. But the fasting blood glucose level was increased >500 mg/dl on the 3rd day some rats (mostly male) were dead 5 days after i.p injection of STZ.
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You should follow mention below point to reduce the death:
1. Should take rats of 3 to 3.5 month old (weight around 250-300 gm)
2. Before induction should put rats on fasting 12-16 hrs.
3.After induction of diabetes should give the sucrose(15g/L) solution for 48 hrs.
3. If blood glucose very high then should give slow acting human insulin of 4-6 U/kg body wt of rats to maintain blood glucose nearly 300 to 350 mg/dL.
I think above point help you in your experiment.
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This question is just out of curiosity and should not be perceived as mindless promotion of strange ideas for diabetes therapy.
Can TRIS, a common base that we all use for preparing buffers be used for prevention of postprandial hyperglycemia or diabetic phenotype contributed by sugar from digestion of disaccharides?
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Thats a good point Mr Apurva Kumar. I will read on this and get back to you
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Some studies particularly in Sweden were done but still nobody can say Diabetes vaccine is produced.
How bacteria and/or transplantation influences on vaccine producing?
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Usually we consider the chemically induced diabetes for experimental purpose to evaluate the antidiabetic activity of herbal drugs and STZ is preferred, but the mechanism of type of diabetes is not clear to me, any suggestions are appreciated.
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Multiple low doses of Streptozotocin will mimic type 1 diabetes, by recruiting immune cells for an immune-mediated apoptotic cell death (see http://www.diacomp.org/shared/showFile.aspx?doctypeid=3&docid=19 for a protocol) A single high dose of streptozotocin will induce massive necrotic cell death. This is falling out of favor as a diabetes model as it does not mimic the pathogenesis of human type 1 diabetes. A single low dose of streptozotocin followed by high-fat diet feeding is one model for type 2 diabetes.