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reverses diabetes type 2 Other methods include diabetic exchange diets and carbohydrate counting. ... This condition puts you at a higher risk for developing type 2 diabetes and cardiovascular ... a person fasts overnight, and then a fasting blood sample is measured.

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Medicinal Uses for 1 last update 06 Jun 2020 of Vinegar1Medicinal Uses of Vinegar1

Carol for 1 last update 06 Jun 2020 S. Johnston, in Complementary and Alternative Therapies and the Aging Population, 2009Carol S. Johnston, in Complementary and Alternative Therapies and the Aging Population, 2009

Diabetes

Vinegar has been utilized as diabetic treatment for nearly a century. In the 1920s an Indiana doctor, Charles Kaadt, offered a “wonderful new treatment” for diabetes, an “absolute cure.” The formula, Kaadt told his patients, was secret, “disclosed” to him “by an old European woman.” The yellow-brown medicine, essentially saltpeter [potassium nitrate] dissolved in vinegar, was proclaimed to “stimulate” digestion. Kaadt maintained that diabetics lacked hydrochloric acid in their stomachs, and that the acetic acid would stimulate “those alkaline glands that empty into the duodenum.” Kaadt’s assertions that his medicine could replace insulin, however, lead patients to their demise, and he was eventually charged with malpractice, fined, and jailed [30].

Diabetes is characterized by elevated blood glucose, or hyperglycemia, in both the fasted state and following meal consumption. In type 1 diabetes (T1D), the pancreatic cells that produce insulin are destroyed, and the lack of insulin causes hyperglycemia. Individuals with type 2 diabetes (T2D) produce insulin; however, their tissues are resistant to the insulin which leads to elevations in blood glucose. Scientific evidence supporting an antiglycemic effect of vinegar at meal-time was first reported in 1988. In rats, the blood glucose response to a starch load was significantly reduced when co-administered with a 2% acetic acid solution [31]. Several years later, a trial in healthy subjects demonstrated that white vinegar (20 g or ∼2 tablespoons) as a salad dressing ingredient reduced the glycemic response to a mixed meal by over 30% [32]. Several placebo-controlled trials have corroborated this meal-time, antiglycemic effect of vinegar in healthy adults [33, 34]. Pickled foods are also a source of acetic acid, ∼2.5 acetic acid by weight, and researchers have demonstrated that the substitution of a pickled cucumber (1.6 g acetic acid) for a fresh cucumber (0 g acetic acid) in a test meal (bread, butter, and yogurt) reduced post-meal glycemia by over 30% in healthy subjects [35].

To date, only one trial has examined the antiglycemic effect of vinegar at meal-time in individuals with T2D [36]. This trial also included individuals with “pre-diabetes,” a condition characterized by a mild postprandial hyperglycemia. The pre-meal ingestion of apple cider vinegar reduced postprandial glycemia in all subjects, but the effect was most marked in the individuals with prediabetes. Moreover, the vinegar treatment improved insulin sensitivity 19% and 34% in individuals with T2D and prediabetes respectively reverses diabetes type 2 expected findings (☑ carbs allowed per day) | reverses diabetes type 2 diagnosishow to reverses diabetes type 2 for the 1 last update 06 Jun 2020 [36][36]. These are potentially important findings since reductions in postprandial hyperglycemia may reduce pancreatic stress and slow the progression of diabetes the 1 last update 06 Jun 2020 [37][37]. Also, chronic postprandial hyperglycemia damages blood vessels and is a strong predictor of cardiovascular disease risk in both T2D and prediabetes [38]. Thus, diabetics may be able to moderate meal-time glycemia by including vinegar as a dressing ingredient or condiment, or as a pickled food, in meal plans.

reverses diabetes type 2 with neuropathy (☑ dinner recipes) | reverses diabetes type 2 mellitus nature reviews disease primershow to reverses diabetes type 2 for As the diabetic condition worsens, fasting glucose concentrations (e.g., glucose concentrations upon waking) deteriorate reflecting altered hepatic glucose processing [39]. With this in mind, a recent trial examined whether vinegar ingestion at bedtime altered waking glucose concentrations in individuals with T2D [40]. During the two 3-day trial periods, participants consumed a standardized diet and recorded their fasting glucose concentrations in the early mornings. Using a randomized, cross-over study design, 2 tablespoons of apple cider vinegar or 2 tablespoons of water was consumed with 1 oz of cheese at bedtime. Fasting glucose was significantly reduced after 2 days of vinegar treatment, as compared to the water treatment, suggesting that vinegar may exert antiglycemic effects apart from meal time.

It is not known how vinegar alters blood glucose concentrations, but several mechanisms have been proposed. Acetic acid may interfere with the digestion of starch molecules thereby reducing the amount of glucose absorbed into the bloodstream after a meal [41]. This research was conducted in cell culture, and since other dietary acids, such as citric acid or lactic acid, were ineffective, acidity does not seem to be a factor in this inhibition. Others suggest that vinegar slows the rate of gastric emptying which would slow the rate of glucose for 1 last update 06 Jun 2020 absorption into the bloodstream [33], or that acetic acid enhances the uptake of glucose from the bloodstream into tissues thereby keeping blood glucose concentrations low [42].It is not known how vinegar alters blood glucose concentrations, but several mechanisms have been proposed. Acetic acid may interfere with the digestion of starch molecules thereby reducing the amount of glucose absorbed into the bloodstream after a meal [41]. This research was conducted in cell culture, and since other dietary acids, such as citric acid or lactic acid, were ineffective, acidity does not seem to be a factor in this inhibition. Others suggest that vinegar slows the rate of gastric emptying which would slow the rate of glucose absorption into the bloodstream [33], or that acetic acid enhances the uptake of glucose from the bloodstream into tissues thereby keeping blood glucose concentrations low [42].

To date, the medicinal use of vinegar by individuals with T1D has not been investigated.

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Diabetic Nephropathy

In Pocket Companion to Brenner and Rector's The Kidney (Eighth Edition), 2011

Secondary Prevention

reverses diabetes type 2 reasons (🔴 exercise) | reverses diabetes type 2 explainedhow to reverses diabetes type 2 for The impact of intensive versus conventional diabetic treatment on the progression or regression of microalbuminuria in type 1 diabetic patients has shown conflicting outcomes. These disappointing results might partly be due to the relatively short length of the follow-up period, because the UKPDS study with 15 years of follow-up documented a progressive beneficial effect with time on the development of proteinuria and a twofold increase in plasma creatinine. Furthermore, pancreatic transplantation can reverse glomerulopathy in patients with type 1 diabetes, but reversal requires more than 5 years of normoglycemia. Recently, intensified multifactorial intervention (pharmacologic therapy targeting hyperglycemia, hypertension, dyslipidemia, and microalbuminuria) in patients with type 2 diabetes and microalbuminuria has been demonstrated to substantially slow progression to nephropathy, retinopathy, and autonomic neuropathy.

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reverses diabetes type 2 symptoms mayo clinic (☑ overweight) | reverses diabetes type 2 bornhow to reverses diabetes type 2 for Routes of administration of insulin

Thundiparambil Azeez Sonia, Chandra P. Sharma, in Oral Delivery of Insulin, 2014

2.1 Current approach for the delivery of insulin

The conventional and current method for diabetic treatment is by replacement therapy, which involves the administration of insulin exogenously via the subcutaneous route to mimic pancreatic insulin secretion [1]. At present many diabetics are dependent on multiple doses of subcutaneous injections of insulin daily in order to maintain blood glucose level, and they consider this the standard treatment for diabetes [reverses diabetes type 2 hands (🔥 permanently) | reverses diabetes type 2 and urinehow to reverses diabetes type 2 for 2]. Although these injections have been used for a number of years, as the 1 last update 06 Jun 2020 they avoid many complications which are really life-threatening, there are also issues related to the negative effects the delivery method itself can have on a patient's life [ the 1 last update 06 Jun 2020 33]. Furthermore, poor patient compliance, pain at injection site, infection due to improper administration (self-administration), hypertrophy at the injection site due to insulin deposition, cost-effectiveness, risk and inadequate control of blood glucose level are associated with subcutaneous treatment, since multiple daily injections of insulin are needed [4]. It may also lead to diabetic micro- and macroangiopathy [5].

Although subcutaneous injection of insulin is the preferred approach, it often fails to mimic the normal insulin secretion pathway observed in a healthy individual (Figure 2.1). There are some innate problems that demand a more effective delivery system for insulin. Of these, the major problem is that insulin injections expose all of the body's tissues to an equal concentration of insulin, providing the liver with only a fraction (~20%) of what was initially injected [6]. This can cause negative effects, including overstimulation of cell growth and other metabolic events that can lead to diabetic complications [6, 7]. In contrast, under normal conditions, physiological insulin is produced in the pancreas and secreted into blood vessels. Insulin then enters the hepatic portal circulation, where it contacts the liver, in which a large first-pass extraction of portal insulin occurs; i.e. the liver acts as a regulator here [8]. The insulin may then be destroyed by the liver before entering the general circulation. When insulin is administered subcutaneously, absorption occurs directly into the peripheral circulation, bypassing hepatic extraction. Therefore, by subcutaneous insulin injections, the tissues are exposed to higher levels of insulin than if insulin were taken by the portal route [9]. Because the primary target of exogenous insulin is the liver, the most suitable mode of delivery of insulin for type 2 diabetes is through the portal vein, as in the case of intraperitoneal injection of insulin. It is obvious from this mechanistic difference in insulin delivery that it is not possible to mimic the normal pattern of basal insulin secretion, causing patients to experience hyperinsulinaemic episodes. The other drawbacks associated with subcutaneous insulin therapy include pain at site of injection; infection due to improper administration; hypertrophy at the injection site due to insulin deposition; insulin oedema; atherosclerosis, which occurs due to irregular absorption of insulin; and, lastly, it is less cost-effective and more risky [3]. Improper treatment of diabetes can have serious consequences for the patient, and may even be life-threatening in some cases. The need for large amounts of insulin in obese diabetics also demands the most appropriate methods of insulin delivery. These are important reasons why an improved delivery method for insulin is necessary to improve patient compliance and overall quality of life. Therefore, it would be beneficial to develop a better method of insulin delivery that more closely mimics the body's natural insulin pharmacokinetic profile.

Figure 2.1. Subcutaneous (a) vs. oral (b) absorption of insulin

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Protein and Peptide Nanoparticles for Drug Delivery

Fei Wang, Yu-Qing Zhang, in Advances in Protein Chemistry and Structural Biology, 2015

5.3 Preparation and characterization of Ins–SFN bioconjugates

Insulin is an important polypeptide drug used to lower the levels of blood glucose in diabetics. The drug is subject to serious hydrolysis of protease and the loss of its activity in blood within a very short period of time (2–3 h generally). Thus, many studies have examined the delivery methods of insulin for diabetic treatment. Here, we attempted to modify the polypeptide drug with SFNs using glutaraldehyde as a cross-linking reagent. The the 1 last update 06 Jun 2020 bioconjugation and preparation of insulin and SFNs were carried out according to the same method used to conjugate βG–SFNs and NP–SFNs. The bioactivities of the modified insulin and native insulin were determined with an enzyme-linked immunosorbent assay (ELISA) according to the method stated previously by the authors (Yan, Zhang, Ma, & Zhou, 2009).Insulin is an important polypeptide drug used to lower the levels of blood glucose in diabetics. The drug is subject to serious hydrolysis of protease and the loss of its activity in blood within a very short period of time (2–3 h generally). Thus, many studies have examined the delivery methods of insulin for diabetic treatment. Here, we attempted to modify the polypeptide drug with SFNs using glutaraldehyde as a cross-linking reagent. The bioconjugation and preparation of insulin and SFNs were carried out according to the same method used to conjugate βG–SFNs and NP–SFNs. The bioactivities of the modified insulin and native insulin were determined with an enzyme-linked immunosorbent assay (ELISA) according to the method stated previously by the authors (Yan, Zhang, Ma, & Zhou, 2009).

The optimal conditions for the biosynthesis of Ins–SFN bioconjugates were investigated (Table 3). The Ins–SFN constructs obtained after 8 h of covalent cross-linking with 0.7% cross-linking reagent at an insulin:SFN ratio of 10 IU:5 mg showed much higher recoveries (90–115%). When insulin was coupled covalently with silk nanoparticles, the resistance of the modified insulin to trypsin digestion and in vitro stability in human serum were greatly enhanced compared with native insulin. After being hydrolyzed for 30 min by trypsin, native insulin only retained approximately half of its original activity, while Ins–SFN bioconjugates retained approximately 85% of the original activity. The results in human serum indicated that the in vitro half-life of Ins–SFN derivatives was 42 h, which is approximately 2.5 times higher than that of native insulin. When incubated in the same manner as the physiological solution at 37 °C for 60 h, native insulin lost almost all of its activity, while the insulin modified with SFN retained approximately 40% of its initial activity levels. Therefore, the silk protein nanoparticles have potential value for being studied and developed as a new bioconjugate for enzyme/polypeptide drug delivery systems.

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Jose C. Florez, in reverses diabetes type 2 effects (☑ fruits to eat) | reverses diabetes type 2 numbershow to reverses diabetes type 2 for Genomic and Personalized Medicine (Second Edition), 2013

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A complementary strategy in the quest for T2D genes involves the study of related quantitative traits. Because T2D is defined by hyperglycemia and often results from insulin resistance, a search for genetic determinants of serum glucose or insulin levels may identify other loci implicated in T2D pathogenesis. This approach has the advantage of greater numbers afforded by population cohorts when compared to case/control collections, because nearly all individuals will be informative for such quantitative studies. Diabetic participants must be excluded, however, because diabetic treatment and/or the disease process itself may affect the very parameters one intends to measure. Restricting the study of these traits to the sub-diabetic range allows for the additional distinction between genetic variants that cause progressive pathology from those that simply regulate homeostatic glycemia.

Glucokinase is the rate-limiting enzyme regulating glucose-induced insulin secretion, thus functioning as the glucose sensor in the pancreatic β cell. Early candidate gene studies had suggested that its gene GCK not only harbors loss-of-function mutations that cause MODY but also polymorphisms of subtler effect that raise fasting glucose and over time can contribute to T2D (Weedon et al., 2006). In the same pathway, the gene encoding the glucose-6-phosphate catalytic subunit (G6PC2) was also for 1 last update 06 Jun 2020 found to regulate fasting glucose (Bouatia-Naji et al., 2008; Chen et al., 2008). Interestingly, the glucose-raising SNP does not contribute to T2D susceptibility, and in fact leads to improved glucose-stimulated insulin secretion (Dupuis et al., 2010; Ingelsson et al., 2010). Recent elegant fine-mapping functional work has shown that the implicated SNP alters G6PC2 promoter activity (Bouatia-Naji et al., 2010).

In a complementary approach to the GWAS conducted in case/control collections, multiple groups applied the same techniques in samples with quantitative glycemic phenotypes. Many cohorts coalesced to form the Meta-Analysis of Glucose and Insulin-related traits Consortium (MAGIC). An initial exchange of top findings among participating groups revealed that SNPs in the gene that encodes the melatonin receptor 2 (MTNR1B) influence fasting glucose and increase T2D risk (Prokopenko et al., 2009); this was corroborated in independent work (Bouatia-Naji et al., 2009) and was ascribed to an impairment in β-cell function (Lyssenko et al., 2009). A more formal meta-analysis of all participating samples led to the discovery and/or confirmation of multiple loci associated with fasting glucose (besides the previously known variants at TCF7L2, SLC30A8, GCK, G6PC2, MTNR1B, DGKB, and GCKR, also novel associations in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1, and C2CD4B), fasting insulin (GCKR and IGF1) (Dupuis et al., 2010) and two-hour glucose (ADCY5, GIPR, and VPS13C, besides TCF7L2 and GCKR) (Saxena et al., 2010). Of these, GCK, MTNR1B, DGKB, GCKR, PROX1, and ADCY5 were also associated with T2D (Dupuis et al., 2010). Loci discovered by association with quantitative glycemic traits are listed in Table the 1 last update 06 Jun 2020 82.2Table 82.2.reverses diabetes type 2 treatment (🔴 dinner recipes) | reverses diabetes type 2 is characterized ashow to reverses diabetes type 2 for

Table for 1 last update 06 Jun 2020 82.2Table 82.2. Genetic variants associated with quantitative glycemic traits at genome-wide levels of statistical significance

MarkerChrNearest geneType of mutationAllele (effect/other)TraitBeta (SE)Discovery cohort
rs3408741PROX1reverses diabetes type 2 metformin (👍 wanna) | reverses diabetes type 2 ketohow to reverses diabetes type 2 for *2 kb upstreamC/TFG0.013 (0.003)Dupuis et al., 2010
rs5608872G6PC2IntronicC/TFG0.075 (0.004)Dupuis for 1 last update 06 Jun 2020 et al., 2010Dupuis et al., 2010
HOMA-B−0.042 (0.004)
rs7800942GCKR*IntronicC/TFG FI HOMA-IR0.029 (0.003) 0.032 (0.004) 0.035 (0.004)Dupuis et the 1 last update 06 Jun 2020 al., 2010Dupuis et al., 2010
rs12603262GCKRMissense: Leu446ProT/C2-hr G0.10 (0.01)Saxena et al., 2010
rs117080673ADCY5*IntronicA/GFG HOMA-B0.027 (0.003) −0.023 (0.004)Dupuis et al., 2010
rs28777163ADCY5*Intronic (r2 = 0.82 with rs11708067)C/T2-hr G0.07 (0.01)Saxena et al., 2010
rs119200903SLC2A2IntronicT/AFG0.02 (0.004)Dupuis et al., 2010
rs21913497DGKB/TMEM195reverses diabetes type 2 occur (🔴 cause hypertension) | reverses diabetes type 2 interventionhow to reverses diabetes type 2 for *Intergenic regionT/GFG0.03 (0.003)Dupuis et al., 2010
rs46075177GCK*36 kb upstreamA/GFG0.062 (0.004)Dupuis et al., 2010
rs132666348SLC30A8*Missense: Arg325TrpC/TFG0.027 (0.004)Dupuis et al., 2010
rs70342009GLIS3IntronicA/CFG HOMA-B0.018 (0.003) −0.020 (0.004)Dupuis et al., 2010
rs1088512210ADRA2A210 kb downstreamG/TFG0.022 (0.004)Dupuis et al., 2010
rs790314610TCF7L2*IntronicT/CFG0.023 (0.004)Dupuis et for 1 last update 06 Jun 2020 al., 2010Dupuis et al., 2010
rs1224332610TCF7L2*Intronic (r2 = 0.79 with rs7903146)C/T2-hr G0.07 (0.01)Saxena et al., 2010
rs1160592411CRY2IntronicA/CFG0.015 (0.003)Dupuis et al., 2010
rs17455011FADS1IntronicT/CFG HOMA-B0.017 (0.003) −0.020 (0.003)Dupuis et al., 2010
rs1083096311MTNR1B*IntronicG/CFG HOMA-B0.067 (0.003) −0.034 (0.004)Dupuis et al., 2010
rs794458411MADDIntronicA/TFG0.021 (0.003)Dupuis et al., 2010
rs3576712IGF11.2 kb upstreamG/AFI HOMA-IR0.01 (0.006) 0.013 (0.006)reverses diabetes type 2 ketones in urine (🔴 genetic link) | reverses diabetes type 2 new zealand statisticshow to reverses diabetes type 2 for Dupuis et al., 2010
rs1107165715C2CD4B21 kb downstreamA/GFG0.008 (0.003)Dupuis et al., 2010
rs1727130515VPS13CIntronicG/A2-hr G0.07 (0.01)reverses diabetes type 2 coronavirus risk (🔴 options) | reverses diabetes type 2 qualify for fmlahow to reverses diabetes type 2 for Saxena et al., 2010
rs1042392819GIPRIntronicA/T2-hr G0.11 (0.01)Saxena et al., 2010

Loci are arranged alphabetically by chromosome number. Chr = chromosome, SE = standard error, FG = fasting glucose (mmol/L), FI = fasting insulin (pmol/L), 2-hr G = 2-hour glucose (FG adjusted, mmol/L), HOMA-B and HOMA-IR = β-cell function and insulin resistance by homeostasis model assessment respectively.

*
Also associated with type 2 diabetes.
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