ArticlePDF Available

Effects Of the Gastric Bypass ALTERNATIVE ® Regimen On Type 1 Diabetes Active Ingredients

Authors:
  • Original Bible Foundation - code2GOD
  • Must Cure Obesity, Inc.

Abstract and Figures

The Gastric Bypass ALTERNATIVE® (a.k.a GBA) regimen is an innovative non-surgical weight reduction regimen with 80,000 users experience in 8 years. The results to date show that successful users are reporting weight reduction at a rate of 2 to 4 times that of bariatric surgery patients. The regimen is made of: > A unique, sophisticated weight analysis to reflect the causes of obesity for each individual > A custom prepared Anti-Cravings, Gastric Bypass EFFECT, reinforcement pills, stress & sleep pills, night pills > A strict boot camp (Facebook.com/groups/LOST100) with 22,000 people managed by Don Karl Juravin > Medical oversight by Dr. Marcus K. Free
Content may be subject to copyright.
v1.1
Mostcomprehensiveresearchstudyon:
EffectsOftheGastricBypass
ALTERNATIVE
®
RegimenOnType1
Diabetes
Authors:RouzbehMotieiLangroudiMD,DonKarl
Juravin(inventor),andMarcusK.FreeMD
Abstract
The Gastric Bypass ALTERNATIVE
®(a.k.a GBA) regimen is an innovative nonsurgical weight
reduction regimen with 80,000 users experience in 8 years. The results to date show that
successful users are reporting weight reduction at a rate of 2 to 4 times that of bariatric
surgerypatients.Theregimenismadeof:
1. Aunique,sophisticatedweightanalysistoreflectthecausesofobesityforeachindividual
2. A custom prepared AntiCravings, Gastric Bypass EFFECT, reinforcement pills, stress &
sleeppills,nightpills 
3. A strict boot camp (Facebook.com/groups/LOST100) with 22,000 people managed by Don
KarlJuravin
4. MedicaloversightbyDr.MarcusK.Free
Study
This research paper discusses the effects of the components of the Gastric Bypass
ALTERNATIVE
®
regimenondiabetes,insulinrelease,andweightloss.
ActiveIngredients
The active ingredients in the Gastric Bypass ALTERNATIVE (a.k.a GBA) regimen are: Beta
Glucan, Camellia Sinensis, Chromium, Fibersol, Green Coffee Bean Extract, Guar Gum,
v1.1
Higenamine Hydrochloric Acid, Inulin, Konjac, Magnesium Stearate, Naringin, Raspberry
Ketones, Silicon Dioxide, Theobromine, Vitamin B6, Vitamin B12, Vitamin D, Willow, Xanthan,
and Yohimbine. Here, we review the existing research articles regarding the effects of each
ingredientontype1orinsulindependentdiabetes.
BetaGlucan
Beta glucan decreases blood glucose without inducing hypoglycemia in type 1
diabetics.
Beta glucan consumption before bedtime decreases blood glucose during early night
hoursintype1diabeticchildrenwithoutinducingnocturnalhypoglycemia(Rami2001).
Beta glucan protects against type 1 diabetes in mice through induction of innate immune
response and modulation of T cell response to pancreatic beta cells (KarumuthilMelethil
2014,Kida1992).
Chromium
Chromium blood level is lower in type 1 diabetics, especially in patients with poor
glycemic control, while chromium intake (200 microg 3 times daily) improves
outcome.
Chromium is involved in insulin signal transduction, insulin and glucose metabolism and
cellularantioxidativedefense(Lin2015,Anderson2000).
Chromium blood level is lower in type 1 diabetics, especially in patients with poor glycemic
control(Gluschenko2016,Lin2015,Karagun2012).
Suboptimal chromium intake increases the risk of diabetes as chromium intake improves
glucoseintoleranceintype1diabetes(Anderson2000).
Chromium picolinate (200 microg 3 times daily for 3 months) decreases HbA1c in type 1
diabetes(Fox1998).
Chromium (200μg) increases insulin sensitivity in individuals with type 1 diabetes and also
permitsreductionsindosagesofinsulinafterjust10days(Chen1997).
v1.1
GuarGum
Guar gum (30 g daily) decreases fasting and postprandial blood glucose (by
19%), hemoglobin A1c (HbA1c, by 0.8) and lowdensitylipoprotein (LDL)    
cholesterol(by20%)intype1diabetics.
Guar gum (4 times per day for 6 weeks) decreases fasting blood glucose, hemoglobin A1c
(HbA1c) and lowdensitylipoprotein (LDL) cholesterol (by 20%) in type 1 diabetics, shown
inarandomizeddoubleblindstudy(VuorinenMarkkola1992).
Guar gum (4 times per day for 4 weeks) decreases blood glucose levels after breakfast
and lunch, daily insulin requirements and serum total cholesterol (by 21%) in type 1
diabetics,showninarandomizeddoubleblindstudy(Ebeling1988).
Guar gum (29 g daily for 1 month) decreases postprandial blood glucose (by 19%) and
HbA1(by0.8)intype1diabetics(Vaaler1986).
Guar gum (5% of daily carbohydrate intake to a maximum of 30 g daily for 3 weeks)
decreases HbA1c, glucosuria and serum total cholesterol in type 1 diabetic children
(Paganus1987).
Naringin
Animal studies show that Naringin does not reduce blood glucose levels in type
1 diabetics, but improves atherogenesis and is helpful in preventing diabetic
ketoacidosis.
Naringin ameliorates cardiac hypertrophy in type 1 diabetic mice by inhibiting oxidative
stress(Adebiyi2016).
Naringin improves plasma insulin, hepatic glycogen content, blood acidity and ketone
bodies but not fasting blood glucose in type 1 diabetic mice. In other words, although
Naringin is not hypoglycemic, it ameliorates ketoacidosis and complications of diabetic
ketoacidosis(Murunga2016).
Naringin is not hypoglycemic in type 1 diabetic rats, but it improves atherogenic index as it
decreases total cholesterol and triglycerides and increases highdensity lipoproteins (HDL)
v1.1
(Xulu2012).
VitaminB6
Vitamin B6 metabolism is altered in type 1 diabetes and its deficiency may
contribute to type I diabetes onset. Conversely, vitamin B6 (100mg daily)  
normalizesendothelialdysfunctionintype1diabetes.
● Vitamin B6 deficiency results in deficient formation of derivatives (like pyridoxal
5'phosphate) necessary for pancreatic islet function and the lack of the derivative may
contribute to the appearance of pancreatic islet autoimmunity and type I diabetes onset  
(Rubi2012).
Vitamin B6 (100mg daily) normalize endothelial dysfunction in type 1 diabetic children, with
theeffectmaintainingover8weeks(MacKenzie2006).
Vitamin B6 metabolism is altered in type 1 diabetes, resulting in its deficiency and diabetic
complications(Masse2012,Kodentsova1994).
VitaminB12
Some type 1 diabetic patients will develop Vitamin B12 deficiency anemia,
obligatingVitaminB12supplementation.
As type 1 diabetes is an autoimmune disease, there is an increased risk of other
autoimmune disorders including pernicious anemia, a type of Vitamin B12deficient anemia
needing lifelong supplementation with Vitamin B12 (De Block 2008, Perros 2000, Davis
1992).
VitaminD
Vitamin D (500 to 4000 IU daily) decreases type 1 diabetes risk by regulating
immunesystemandcalciumhomeostasisanditsdirecteffectonbetacells.
Vitamin D deficiency increases the incidence of type 1 diabetes. Conversely, early and
longterm vitamin D supplementation decreases diabetes risk by regulating immune
system and calcium homeostasis and its direct effect on beta cells that renders them more
v1.1
resistant to cellular stress (Griz 2014, Badenhoop 2012, WoldenKirk 2011, Hypponen
2010,Luong2005,Mathieu2005a,Mathieu2005b).
High dose Vitamin D (50 microg or 2000 IU daily) but not low dose (10 microg or 400 IU
daily)haveastrongprotectiveeffectontype1diabetes(Harris2005,Harris2002).
Vitamin D supplementation during early life (infancy) decreases type 1 diabetes risk during
laterlifeby29%(Dong2013,Zipitis2008).
Below normal vitamin D levels are observed in 71% of type 1 diabetic individuals.
Moreover, insulin requirement is higher in type 1 diabetics with decreased serum vitamin D
levels(Thnc2011,Holick2005).
Higher vitamin D levels are associated with lower HbA1c levels in type 1 diabetics (Al
Sawah2016).
Vitamin D supplementation (4000 IU daily) improves HbA1c after 12 weeks in vitamin
Ddeficienttype1diabetics(Aljabri2010).
Vitamin D deficiency predisposes to type 1 diabetes, while Vitamin D supplementation (500
IUto1000IUdaily)preventthedisease(Mathieu2015).
Vitamin D supplementation influences immune regulation and subsequently may prevent
progressiontotype1diabetesingeneticallysusceptibleindividuals(Harinarayan2014).
References
1. Adebiyi,A.,Adebiyi,O.,Owira,P.(2016).NaringinMitigatesCardiacHypertrophybyReducingOxidative
StressandInactivatingcJunNuclearKinase1ProteininTypeIDiabetes.JournalofCardiovascular
Pharmacology[online],67(2),pp.13644.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/26421421
[Accessed06.01.2017].
2. Aljabri,K.,Bokhari,S.,Khan,M.(2010).GlycemicchangesaftervitaminDsupplementationinpatientswith
type1diabetesmellitusandvitaminDdeficiency.AnnalsofSaudiMedicine[online],30(6),pp.4548.
Availablefrom:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994161/[Accessed04.01.2017].
3. AlSawah,S.,Compher,C.,Hanlon,A.,etal.(2016).25HydroxyvitaminDandglycemiccontrol:A
crosssectionalstudyofchildrenandadolescentswithtype1diabetes.DiabetesResearchandClinical
Practice[online],115,pp.549.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/27242123[Accessed
05.01.2017].
4. Anderson,R.(2000).Chromiuminthepreventionandcontrolofdiabetes.DiabetesandMetabolism[online],
26(1),pp.227.Availablefrom:http://www.emconsulte.com/article/79857/alertePM[Accessed28.12.2016].
5. Badenhoop,K.,Kahles,H.,PennaMartinez,M.(2012).VitaminD,immunetolerance,andpreventionoftype
1diabetes.CurrentDiabetesReports[online],12(6),pp.63542.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/22976537[Accessed05.01.2017].
v1.1
6. Chen,S.,Sun,Y.,Chen,X.(1997).Effectofjiangtangkangonbloodglucose,sensitivityofinsulinandblood
viscosityinnoninsulindependentdiabetesmellitus[inChinese].ZhongguoZhongXiYiJieHeZaZhi,17,
pp.666–8.Availablefrom:http://www.ncbi.nlm.nih.gov/pubmed/10322847[Accessed02.06.2016].
7. Davis,R.,McCann,V.,Stanton,K.(1992).Type1diabetesandlatentperniciousanaemia.TheMedical
JournalofAustralia[online],156(3),pp.1602.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/1545717[Accessed28.12.2016].
8. DeBlock,C.,DeLeeuw,I.,VanGaal,L.(2008).Autoimmunegastritisintype1diabetes:aclinicallyoriented
review.JournalofClinicalEndocrinologyandMetabolism[online],93(2),pp.36371.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/18029461[Accessed28.12.2016].
9. Dong,J.,Zhang,W.,Chen,J.,etal.(2013).VitaminDintakeandriskoftype1diabetes:ametaanalysisof
observationalstudies.Nutrients[online],5(9),pp.355162.Availablefrom:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798920/[Accessed05.01.2017].
10. Ebeling,P.,YkiJärvinen,H.,Aro,A.,etal.(1988).Glucoseandlipidmetabolismandinsulinsensitivityin
type1diabetes:theeffectofguargum.AmericanJournalofClinicalNutrition[online],48(1),pp.98103.
Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/3291601[Accessed27.12.2016].
11. Fox,G.,Sabovic,Z.(1998).Chromiumpicolinatesupplementationfordiabetesmellitus.TheJournalof
FamilyPractice[online],46(1),pp.836.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/9451374
[Accessed28.12.2016].
12. Gluschenko,N.,Vasylyshyn,K.,Roschupkin,A.,etal.(2016).Thecontentofmicroelementsinbloodserum
anderythrocytesinchildrenwithdiabetesmellitustypeIdependingonlevelofglycemiccontrol.Georgian
MedNews[online],250,pp.6671.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/26870978
[Accessed28.12.2016].
13. Griz,L.,Bandeira,F.,Gabbay,M.,etal.(2014).VitaminDanddiabetesmellitus:anupdate2013.Arquivos
BrasileirosdeEndocrinologiaeMetabologia[online],58(1),pp.18.Availablefrom:
http://www.scielo.br/pdf/abem/v58n1/00042730abem5810001.pdf[Accessed05.01.2017].
14. Harinarayan,C.(2014).VitaminDanddiabetesmellitus.Hormones[online],13(2),pp.16381.Available
from:http://www.hormones.gr/8472/article/article.html[Accessed04.01.2017].
15. Harris,S.(2005).VitaminDintype1diabetesprevention.JournalofNutrition[online],135(2),pp.3235.
Availablefrom:http://jn.nutrition.org/content/135/2/323.long[Accessed05.01.2017].
16. Harris,S.(2002).CanvitaminDsupplementationininfancypreventtype1diabetes?NutritionReviews
[online],60(4),pp.11821.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/12002683[Accessed
05.01.2017].
17. Holick,M.(2005).VitaminD:importantforpreventionofosteoporosis,cardiovascularheartdisease,type1
diabetes,autoimmunediseases,andsomecancers.SouthernMedicalJournal[online],98(10),pp.10247.
Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/16295817[Accessed05.01.2017].
18. Hyppönen,E.(2010).VitaminDandincreasingincidenceoftype1diabetesevidenceforanassociation?
DiabetesObesityandMetabolism[online],12(9),pp.73743.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/20649624[Accessed05.01.2017].
19. Karagun,B.,Temiz,F.,Ozer,G.,etal.(2012).Chromiumlevelsinhealthyandnewlydiagnosedtype1
diabeticchildren.PediatricsInternational[online],54(6),pp.7805.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/22783884[Accessed28.12.2016].
20. KarumuthilMelethil,S.,Gudi,R.,Johnson,B.,etal.(2014).Fungalβglucan,aDectin1ligand,promotes
v1.1
protectionfromtype1diabetesbyinducingregulatoryinnateimmuneresponse.JournalofImmunology
[online],193(7),pp.330821.Availablefrom:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4170060/
[Accessed27.12.2016].
21. Kida,K.,Inoue,T.,Kaino,Y.,etal.(1992).Animmunopotentiatorofbeta1,6;1,3Dglucanpreventsdiabetes
andinsulitisinBBrats.DiabetesResearchandClinicalPractice[online],17(2),pp.759.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/1425150[Accessed28.12.2016].
22. Kodentsova,V.,Vrzhesinskaia,O.,Sokol'nikov,A.,etal.(1994).Vitaminmetabolisminchildrenwith
insulindependentdiabetesmellitus.Effectoflengthofillness,severity,anddegreeofdisruptionofsubstance
metabolism.VoprosyMeditsinskoiKhimii[online],40(4),pp.338.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/7975378[Accessed04.01.2017].
23. Lin,C.,Huang,Y.(2015).Chromium,zincandmagnesiumstatusintype1diabetes.CurrentOpinionin
ClinicalNutritionandMetabolicCare[online],18(6),pp.58892.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/26406393[Accessed28.12.2016].
24. Luong,K.,Nguyen,L.,Nguyen,D.(2005).TheroleofvitaminDinprotectingtype1diabetesmellitus.
DiabetesMetabolismResearchandReviews[online],21(4),pp.33846.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/15852446[Accessed05.01.2017].
25. MacKenzie,K.,Wiltshire,E.,Gent,R.,etal.(2006).FolateandvitaminB6rapidlynormalizeendothelial
dysfunctioninchildrenwithtype1diabetesmellitus.Pediatrics[online],118(1),pp.24253.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/16818571[Accessed29.12.2016].
26. Massé,P.,Boudreau,J.,Tranchant,C.,etal.(2012).Type1diabetesimpairsvitaminB(6)metabolismatan
earlystageofwomen'sadulthood.AppliedPhysiologyNutritionandMetabolism[online],37(1),pp.16775.
Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/22288928[Accessed29.12.2016].
27. Mathieu,C.(2015).VitaminDanddiabetes:Wheredowestand?DiabetesResearchandClinicalPractice
[online],108(2),pp.2019.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/25700626[Accessed
04.01.2017].
28. Mathieu,C.,Badenhoop,K.(2005a).VitaminDandtype1diabetesmellitus:stateoftheart.Trendsin
EndocrinologyandMetabolism[online],16(6),pp.2616.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/15996876[Accessed05.01.2017].
29. Mathieu,C.,Gysemans,C.,Giulietti,A.,etal.(2005b).VitaminDanddiabetes.Diabetologia[online],48(7),
pp.124757.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/15971062[Accessed05.01.2017).
30. Murunga,A.,Miruka,D.,Driver,C.,etal.(2016).GrapefruitDerivedFlavonoidNaringinImproves
KetoacidosisandLipidPeroxidationinType1DiabetesRatModel.PLoSOne[online],11(4),pp.e0153241.
Availablefrom:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4830547/[Accessed06.01.2017].
31. Paganus,A.,Mäenpää,J.,Akerblom,H.,etal.(1987).Beneficialeffectsofpalatableguarandguarplus
fructosedietsindiabeticchildren.ActaPaediatricaScandinavica[online],76(1),pp.7681.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/3551494[Accessed27.12.2016].
32. Perros,P.,Singh,R.,Ludlam,C.,etal.(2000).PrevalenceofperniciousanaemiainpatientswithType1
diabetesmellitusandautoimmunethyroiddisease.DiabeticMedicine[online],17(10),pp.74951.Available
from:https://www.ncbi.nlm.nih.gov/pubmed/11110510[Accessed28.12.2016].
33. Rami,B.,Zidek,T.,Schober,E.(2001).Influenceofabetaglucanenrichedbedtimesnackonnocturnal
bloodglucoselevelsindiabeticchildren.JournalofPediatricGastroenterologyandNutrition[online],32(1),
pp.346.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/11176321[Accessed27.12.2016].
v1.1
34. Rubí,B.(2012).Pyridoxal5'phosphate(PLP)deficiencymightcontributetotheonsetoftypeIdiabetes.
MedicalHypotheses[online],78(1),pp.17982.https://www.ncbi.nlm.nih.gov/pubmed/22088923[Accessed
29.12.2016].
35. Thnc,O.,Cetinkaya,S.,Kizilgün,M.,etal.(2011).VitaminDstatusandinsulinrequirementsinchildrenand
adolescentwithtype1diabetes.JournalofPediatricEndocrinologyandMetabolism[online],24(1112),pp.
103741.Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/22308861[Accessed05.01.2017].
36. Vaaler,S.,Hanssen,K.,DahlJørgensen,K.,etal.(1986).Diabeticcontrolisimprovedbyguargumand
wheatbransupplementation.DiabeticMedicine[online],3(3),pp.2303.Availablefrom:
https://www.ncbi.nlm.nih.gov/pubmed/3030619[Accessed27.12.2016].
37. VuorinenMarkkola,H.,Sinisalo,M.,Koivisto,V.(1992).Guargumininsulindependentdiabetes:effectson
glycemiccontrolandserumlipoproteins.AmericanJournalofClinicalNutrition[online],56(6),pp.105660.
Availablefrom:https://www.ncbi.nlm.nih.gov/pubmed/1442657[Accessed27.12.2016].
38. WoldenKirk,H.,Overbergh,L.,Christesen,H.,etal.(2011).VitaminDanddiabetes:itsimportanceforbeta
cellandimmunefunction.MolecularandCellularEndocrinology[online],347(12),pp.10620.Available
from:https://www.ncbi.nlm.nih.gov/pubmed/21889571[Accessed05.01.2017].
39. Xulu,S.,OromaOwira,P.(2012).Naringinamelioratesatherogenicdyslipidemiabutnothyperglycemiain
ratswithtype1diabetes.JournalofCardiovascularPharmacology[online],59(2),pp.13341.Available
from:https://www.ncbi.nlm.nih.gov/pubmed/21964158[Accessed06.01.2017].
40. Zipitis,C.,Akobeng,A.(2008).VitaminDsupplementationinearlychildhoodandriskoftype1diabetes:a
systematicreviewandmetaanalysis.ArchivesofDiseaseinChildhood[online],93(6),pp.5127.Available
from:http://adc.bmj.com/content/93/6/512.full.pdf+html[Accessed05.01.2017].
Footnote
ThisresearchwassponsoredbyMustCureObesityCO.(Florida2000)
DonKarlJuravinistheinventor
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
Background: Hypoglycemic effects of grapefruit juice are well known but the effects of naringin, its main flavonoid on glucose intolerance and metabolic complications in type 1 diabetes are not known. Objectives: To investigate the effects of naringin on glucose intolerance, oxidative stress and ketonemia in type 1 diabetic rats. Methods: Sprague-Dawley rats divided into 5 groups (n = 7) were orally treated daily with 3.0 ml/kg body weight (BW)/day of distilled water (group 1) or 50 mg/kg BW of naringin (groups 2 and 4, respectively). Groups 3, 4 and 5 were given a single intra-peritoneal injection of 60 mg/kg BW of streptozotocin to induce diabetes. Group 3 was further treated with subcutaneous insulin (4.0 IU/kg BW) twice daily, respectively. Results: Stretozotocin (STZ) only-treated groups exhibited hyperglycemia, polydipsia, polyuria, weight loss, glucose intolerance, low fasting plasma insulin and reduced hepatic glycogen content compared to the control group. Furthermore they had significantly elevated Malondialdehyde (MDA), acetoacetate, β-hydroxybutyrate, anion gap and significantly reduced blood pH and plasma bicarbonate compared to the control group. Naringin treatment significantly improved Fasting Plasma Insulin (FPI), hepatic glycogen content, malondialdehyde, β-hydroxybutyrate, acetoacetate, bicarbonate, blood pH and anion gap but not Fasting Blood Glucose (FBG) compared to the STZ only-treated group. Conclusions: Naringin is not hypoglycemic but ameliorates ketoacidosis and oxidative stress. Naringin supplements could therefore mitigate complications of diabetic ketoacidosis.
Article
Full-text available
Cardiac hypertrophy (CH) in type 1 diabetes mellitus is attributed to increased oxidative stress associated activation of c-Jun Nuclear Kinase (JNK). We investigated the effects of naringin on hyperglycemia-associated oxidative stress, activation of JNK-1 and CH.Male Sprague-Dawley rats (225-250 g) (n=7) were divided into 6 groups. Groups I and II were orally treated with distilled water [3.0 ml/kg bodyweight/day (BW)] and naringin (50 mg/kg BW), respectively. Groups III-VI were rendered diabetic by a single i.p injection of 65 mg/kg BW of streptozotocin (STZ). Groups III, IV and V were further treated with insulin (4.0 I.U, s.c, twice daily), naringin (50 mg/kg BW) and ramipril (3.0 mg/kg BW), respectively.After 56 days, the animals were sacrificed then plasma and cardiac tissues obtained for further analysis. Naringin treatment of diabetic rats significantly reversed oxidative stress, lipid peroxidation, proteins oxidation, cardiac hypertrophy indices, and JNK protein activation compared to untreated diabetic animals. Our results do suggest that naringin mitigates cardiac hypertrophy by inhibiting oxidative stress leading to inactivation of JNK-1. Naringin supplements could therefore ameliorate CH in diabetic patients.
Article
Full-text available
Vitamin D deficiency and diabetes mellitus are two common conditions and they are widely prevalent across all ages, races, geographical regions, and socioeconomic conditions. Epidemiologic studies have shown association of vitamin D deficiency and increased risk of chronic diseases, such as cancer, cardiovascular disease, type 2 diabetes, and autoimmune diseases, such as multiple sclerosis and type 1 diabetes mellitus. The identification of 1,25(OH)2D receptors and 1-α-hydroxilase expression in pancreatic beta cells, in cells of the immune system, and in various others tissues, besides the bone system support the role of vitamin D in the pathogenesis of type 2 diabetes. Observational studies have revealed an association between 25(OH) D deficiency and the prevalence of type 1 diabetes in children and adolescents. This review will focus on the concept of vitamin D deficiency, its prevalence, and its role in the pathogenesis and risk of diabetes mellitus and cardiovascular diseases.
Article
Full-text available
Vitamin D is suggested to have protective effects against type 1 diabetes. However, the results from observational studies have been inconsistent. We aimed to examine their association by conducting a meta-analysis of observational studies. Multiple databases were searched in June 2013 to identify relevant studies including both case-control and cohort studies. Either a fixed- or random-effects model was used to calculate the pooled risk estimate. We identified eight studies (two cohort studies and six case-control studies) on vitamin D intake during early life and three studies (two cohort studies and one case-control study) on maternal vitamin D intake during pregnancy. The pooled odds ratio for type 1 diabetes comparing vitamin D supplementation with non-supplementation during early life was 0.71 (95% confidence interval [CI], 0.51-0.98). Similar results were observed in the case-control subgroup analysis but not in the cohort subgroup analysis. The pooled odds ratio with maternal intake of vitamin D during pregnancy was 0.95 (95% CI, 0.66-1.36). In conclusion, vitamin D intake during early life may be associated with a reduced risk of type 1 diabetes. However, there was not enough evidence for an association between maternal intake of vitamin D and risk of type 1 diabetes in the offspring.
Article
Aim: The objective of this study was to describe the vitamin D status of children and adolescents with type 1 diabetes and to evaluate whether levels of 25-hydroxyvitamin D are significantly associated with HbA1c in this population. Methods: 197 children and adolescents from a diabetes center in a children's hospital were recruited during regular follow up visit. Non-fasting blood samples were collected to measure 25-hydroxyvitamin D and blood glucose levels. HbA1c and other key variables were abstracted from patients' medical records. Results: Of the 197 children and adolescents, more than half were adolescents, males, and Caucasian. 23% were overweight, while 13% were obese. Mean HbA1c was 8.6±1.4% (70±15.3mmol/mol). 40.6% of patients had 25-hydroxyvitamin D levels ≤50nmol/L; 49.2% had 25-hydroxyvitamin D levels between 51 and 75nmol/L and 10.2% had 25-hydroxyvitamin D levels >75nmol/L. The bivariate relationship between 25-hydroxyvitamin D and HbA1c almost reached statistical significance (P=0.057), while no significance was established in the multivariate model. Conclusions: To the best of our knowledge this is the first study that has been adequately-powered to examine the association between 25-hydroxyvitamin D and HbA1c in children and adolescents with T1DM. This study demonstrated the high prevalence of patients with low levels of 25-hydroxyvitamin D specifically in healthy weight and Caucasian children and adolescents with T1DM. These data suggest the need for monitoring of 25-hydroxyvitamin D in all youth with T1DM.
Article
The aim of this paper is to investigate the content of chromium, cobalt and nickel in serum and erythrocytes in children with type 1 diabetes mellitus, depending on the level of glycemic control. The study was conducted on 68 children with type 1 diabetes mellitus. The patients were divided into four groups based on glycemic control. Group I was composed of 9 children with optimal level of glycemic control. Group II - 25 children with suboptimal level of glycemic control. Group III - 34 children with a high risk to life level of glycemic control. Group IV (control group) consisted of 30 healthy children. Compensation state of type 1 diabetes was evaluated according to ISPAD (Consensus for the Management of Type 1 Diabetes Mellitus in Children and Adolescens 2000). The content of trace elements in biological agents was determined by atomic absorbtion spectrophotometry method with C-115M1 mass-spectrophotometer, manufactured by «Selmi» enterprise (Ukraine). It is found that there is a decrease in serum concentrations of chromium and erythrocyte content of cobalt in patients with optimal level of glycemic control. The deficiency of chromium is accompanied by the deficiency of cobalt in patients with suboptimal level of glycemic control. The lower levels of cobalt and nickel are recorded simultaneously, but there is theexcess of chromium in the erythrocytes of these patients. Patients, who suffer from 1 type diabetes mellitus and high risk for life level of glycemic control have considerable polideficiency of cobalt, nickel and chromium in serum.The increasing level of chromium was recorded only in the erythrocytes. The level of glycemic control and the duration of 1 type diabetes mellitus are important in the forecasting of the development of chronic diabetic complications. It is found that the duration of 1 type diabetes mellitus influences the levels of cobalt and nickel in serum mostly, while the level of glycemic control influences the chromium content.
Article
The vitamin D endocrine system in now recognized as subserving a wide range of fundamental biological functions in cell differentiation, inhibition of cell growth as well as immunomodulation. Both forms of immunity, namely adaptive and innate, are regulated by 1,25(OH)2D3. The immune-modulatory properties of vitamin D suggest that it could play a potential therapeutic role in prevention of type 1 diabetes mellitus (T1DM). It is postulated that large doses of vitamin D supplementation may influence the pattern of immune regulation and subsequent progression to T1DM in a genetically susceptible individual. More studies are required to substantiate the relation between T1DM and vitamin D/vitamin D analogues in the pattern of immune regulations in susceptible individuals. In type 2 diabetes mellitus (T2DM), vitamin D may influence both insulin secretion and sensitivity. An inverse relationship between T2DM and vitamin D is postulated from cross-sectional and prospective studies, though conclusive proof is as yet lacking. Available studies differ in their design and in the recommended daily allowances (RDA) of vitamin D in non-skeletal diseases and β-cell function. Large, well designed, controlled, randomized interventional studies on the potential role of vitamin D and calcium in prevention and management of T2DM are required to clarify the relationship between vitamin D and glucose homeostasis in T2DM.
Article
Vitamin D is a secosteroid hormone that resembles other nuclear steroid hormones such as thyroid, gluco-, and mineralocorticoids, as well as gonadal effector systems. Primarily understood as a master regulator of bone and calcium/phosphate physiology, it is now increasingly recognized as orchestrating numerous aspects of cell growth and differentiation in many tissues, including those of innate and acquired immunity. This review addresses recently discovered aspects that highlight vitamin D´s potential for immune intervention and how the vitamin D pathway is utilized for anti-infective and antineoplastic immunity. This provides the rationale for novel therapeutic strategies in the context both of prevention and of therapy of immune dysregulation in type 1 diabetes.
Article
Background: The aim of this study was to compare the chromium levels of plasma (PCL), erythrocyte (ECL) and urine (UCL) in type 1 diabetics and healthy subjects and to review the relation between metabolic parameters. Methods: We evaluated 165 subjects who were: newly diagnosed type 1 diabetics (group 1 [n= 29]); previously diagnosed type 1 diabetics (group 2 [n= 18]); non-diabetic control subjects who were admitted and treated for any reason in hospital (group 3 [n= 21]); and two other groups of control subjects from two schools that have different socioeconomic levels (group 4 [n= 48] and group 5 [n= 49]). Results: PCL in group 1 and group 2 subjects (7.21 ± 4.78 and 10.94 ± 3.04 mcg/L, respectively) was significantly lower than in all control groups (21.84 ± 7.87, 16.11 ± 7.44, 17.25 ± 8.58 mcg/L, respectively) (P < 0.05). A significant difference in PCL between the group 1 and group 2 subjects was present (7.21 ± 4.78 and 10.94 ± 3.04, respectively) (P= 0.021). ECL (as tissue chromium) in group 1 and group 2 subjects (13.99 ± 11.37 and 19.64 ± 12.58, respectively) was significantly lower than in all control groups (28.20 ± 7.34.25, 49 ± 12.47, 26.37 ± 9.77 mcg/L, respectively) (P= 0.05). UCL in group 1 and group 2 subjects (11.44 ± 6.88 and 15.68 ± 6.75 mcg/L, respectively) was significantly lower than in group 3 subjects (28.83 ± 9.37 mcg/L) (P < 0.05). There were significant correlations between length, bodyweight and PCL in the group 1 subjects (r = 0.42, P= 0.22 and r = 0.53, P= 0.03, respectively). There was a negative correlation between plasma glucose and UCL, which was not statistically significant in group 2 subjects (r =-0.4, P= 0.061). Conclusion: There was a negative chromium balance in type 1 diabetics. This negative balance may affect the insulin function badly. If this negative balance should be confirmed by recent studies we suggest that chromium supplementation with insulin is necessary for type 1 diabetes.
Article
Vitamin D and its active form are potent immunomodulators and are known to play an important role in the glucose/insulin metabolism. Studies on type 2 diabetes mellitus (T2DM) have shown that vitamin D increases insulin efficacy; however, there are no studies that define a similar relationship in type 1 diabetes mellitus (T1DM). The aim of this study was to investigate the relation between serum vitamin D levels and the insulin requirement used in children with T1DM. A total of 100 patients with T1DM aged 4.7-19.9 years were included in the study. Serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, 25-hydroxyvitamin D (25OHD), and 1,25-dihydroxyvitamin D were measured. A serum 25OHD level of < 10 ng/mL was accepted as vitamin D deficiency, whereas < 20 ng/mL was accepted as vitamin D insufficiency. We found vitamin D deficiency in 28% and vitamin D insufficiency in 43% of our patients, whereas 29% had normal serum 25OHD levels. The insulin requirement of patients with a serum 25OHD level below 10 ng/mL were significantly higher than those of patients with a serum 25OHD level above 10 ng/mL (p = 0.012). This result did not change in those with diabetes duration of over 1 year. There was weak correlation between the daily insulin requirements and serum vitamin D levels (r = -0.212, p = 0.032). We found a significantly higher insulin requirement in T1DM children with decreased serum 25OHD levels and decreased insulin sensitivity. We recommend checking the level of serum 25OHD in children with diabetes and starting treatment if it is deficient/inadequate.