Preparation of Nanocomposite Peptide and Its Inhibitory Effect on Myocardial Injury in Type-II Diabetic Rats

2021 ◽  
Vol 21 (2) ◽  
pp. 1378-1384
Author(s):  
Yang Zhang ◽  
Shaowei Zhuang ◽  
Shengyang Jiang ◽  
Jiehan Zhang ◽  
Yu Chen
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Cardiomyopathy ◽  
Myocardial Injury ◽  
Drug Carrier ◽  
Systolic Dysfunction ◽  
Experimental Studies ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Peptide Drugs

Complications of diabetes are the main cause of death and disability in diabetic patients. Cardiovascular diseases, especially diabetic cardiomyopathy, are one of the major complications and causes of death in type 2 diabetes. Peptide drugs have a better effect on improving cellular oxidative damage, reducing tissue inflammation and inhibiting intracellular calcium overload. The application of nanotechnology to the preparation of peptide drugs and myocardial injury can effectively improve myocardial stun, arrhythmia and myocardial systolic dysfunction in patients with type 2 diabetes. The use of nanotechnology to develop more stable Glucagon-like peptide 1 analogues or sustained-release preparations, improve patient compliance and improve the efficacy of diabetes, is of great significance for the prevention and treatment of diabetic cardiomyopathy. Therefore, this study used nanotechnology to prepare PLGA-GLP-1 nanoparticles using polyglycolic acid glycolic acid as a drug carrier, which achieved long-acting drug and its morphology by transmission electron microscopy. At the same time, this study explored the anti-cardiomyocyte injury and anti-myocardial damage of PLGA-GLP-1 nanocomposite peptide and its molecular mechanism by using animal models and cell models. Experimental studies have shown that PLGA-GLP-1 nanocomposite peptide has a protective effect on myocardial injury in diabetic rats. Its mechanism is related to the PLGA-GLP-1 nanocomposite peptide enhancing the body’s antioxidant capacity, anti-cardiomyocyte apoptosis, and promoting mitochondrial DNA repair in cardiomyocytes.

P0751METFORMIN, A CLASSIC TREATMENT FOR TYPE 2 DIABETES WITH POSSIBLE RENOPROTECTIVE EFFECTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Adriana Acosta Barrios ◽  
Marian Goicoechea ◽  
Eduardo Verde ◽  
Ángela González-Rojas ◽  
Andres Delgado ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Kidney Disease ◽  
Experimental Studies ◽  
Diabetic Patients ◽  
Metformin Treatment ◽  
End Point ◽  
Progression Of Kidney Disease

Abstract Background and Aims Metformin is the antidiabetic of choice in patients with type 2 diabetes mellitus. Experimental studies and clinical observations have shown that metformin could have a beneficial effect on the progression of kidney disease through the activation of cAMP due to its anti-inflammatory, antifibrotic, and anti-oxidative action. The objective was to compare the progression of CKD in diabetic patients with or without metformin as antidiabetic in their treatment and the prevalence of cardiovascular events in both groups. Method Unicentric retrospective observational analysis. Inclusion criteria: outpatients seen in nephrology consultation during the year of 2012 with diabetes mellitus and stage 3 CKD. Renal, cardiovascular outcomes and mortality were analyzed between patients treated with / without metformin. Median follow-up of 76.5 months (41-84). Renal end-point: estimated glomerular filtration rate drop (MDRD-4) by 50% and / or start of dialysis program. Cardiovascular end-point: ischemic heart disease, stroke, arterial revascularization and / or amputation. Cardiovascular or any cause mortality. Results 148 patients (96M, 52W) with a mean age of 75±9 years and an eGFR of 40±9 ml / min / 1.73 m2 were included. In relation to hypoglycemic therapy: 45 received metformin, 61 insulin and 31 DPP4i. 80% received treatment with RAAS blockers. After the follow-up, the progression of the renal disease was greater in patients who did not receive metformin: eGFR fall of -7.0±16 vs -0.15±16 ml / min in those treated with metformin (p = 0.019). 25 patients in the group without metformin suffered a renal event vs. 5 in the metformin group (logRank: 4.186, p = 0.045). In the Cox analysis, metformin treatment decreases the progression of kidney disease in a model adjusted for baseline renal function and treatment with RAASB (HR 0.368, p = 0.043), losing its predictive power in a proteinuria-adjusted model. During the follow-up, 45 patients died (20 metformin, 25 non-metformin) and 45 patients suffered a cardiovascular event (15 metformin, 30 non-metformin), with no differences between the two groups. Conclusion Metformin treatment in patients with stage 3 CKD could slow the progression of CKD, this effect should be demonstrated in randomized studies with larger sample size.

scholarly journals Probiotics ameliorate pioglitazone-associated bone loss in diabetic rats

2020 ◽  
Author(s):  
Ahmad Gholami ◽  
Mohammad Hossein Dabbaghmanesh ◽  
Younes Ghasemi ◽  
Pedram Talezadeh ◽  
Farhad Koohpeyma ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Bone Loss ◽  
Lactobacillus Reuteri ◽  
Diabetic Rats ◽  
Urinary Calcium ◽  
Diabetic Patients ◽  
Protective Effects

Abstract Background Pioglitazone as a PPAR-g agonist are used for management of type 2 diabetes mellitus. Nevertheless, evidence showed that the therapeutic modulation of PPARg activity using Pioglitazone may be linked with bone mass reduction and fracture risk in type 2 diabetes mellitus patients. The objective of the current research was to inspect the preventive role of some types of probiotic strains including ( Lactobacillus acidophilus , Lactobacillus reuteri , Lactobacillus casei , Bifidiobacterum longum and Bacillus coagulans ) against pioglitazone-induced bone loss. Methods Streptozotocin (60 mg/kg) was administered for diabetes induction. Diabetic rats were fed orally with pioglitazone (300 mg/kg) and probiotics (1×109 CFU/ml/day) alone and in combination of both for 4 weeks. Dual energy X-ray absorptiometry (DEXA) were used to asses BMD, BMC and area of the femur, spine and tibia at the experiment termination. Serum glucose, serum calcium, alkaline phosphatase, phosphorus, BUN, Creatinine, and urine calcium were also analyzed. Results Administration of pioglitazone and probiotics alone and in combination significantly improved elevated blood glucose. Pioglitazone treatment significantly increased urinary calcium and BUN, and decreased ALP and creatinine. Co-treatment of probiotics with pioglitazone significantly decreased urinary calcium, creatinine and ALP. Pioglitazone showed detrimental effects on femur-BMD whereas treatment with probiotics remarkably ameliorated these effects. Among the tested probiotics Bifidiobacterum longum displayed the best protective effects on pioglitazone-induced bone loss in diabetic rats. Conclusion This study suggests probiotic supplementation in diabetic patients on pioglitazone regime could be considering as a good strategy to ameliorate bone loss induced by pioglitazone.

scholarly journals Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ying-Ying Tan ◽  
Lei-Xin Chen ◽  
Ling Fang ◽  
Qi Zhang
Keyword(s):  
Nadph Oxidase ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Myocardial Injury ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Therapeutic Effects ◽  
H9c2 Cells ◽  
Cardioprotective Effects

Abstract Background Diabetic cardiomyopathy is a main cause of the increased morbidity in diabetic patients, no effective treatment is available so far. Polydatin, a resveratrol glucoside isolated from the Polygonum cuspidatum, was found by our and others have antioxidant and cardioprotective activities. Therapeutic effects of polydatin on diabetic cardiomyopathy and the possible mechanisms remains unclear. This study aimed to investigate the cardioprotective effects and underlying mechanisms of polydatin on myocardial injury induced by hyperglycemia. Methods Diabetes in rats was made by high-fat diet combined with multiple low doses of streptozotocin, and then treated with polydatin (100 mg·kg-1·day-1, by gavage) for 8 weeks. Cardiac function was examined by echocardiography. Myocardial tissue and blood samples were collected for histology, protein and metabolic characteristics analysis. In cultured H9c2 cells with 30 mM of glucose, the direct effects of polydatin on myocyte injury were also observed. Results In diabetic rats, polydatin administration significantly improved myocardial dysfunction and attenuated histological abnormalities, as evidenced by elevating left ventricular shortening fraction and ejection fraction, as well as reducing cardiac hypertrophy and interstitial fibrosis. In cultured H9c2 cells, pretreatment of polydatin dose-dependently inhibited high glucose-induced cardiomyocyte injury. Further observation evidenced that polydatin suppressed the increase in the reactive oxygen species levels, NADPH oxidase activity and inflammatory cytokines production induced by hyperglycemia in vivo and in vitro. Polydatin also prevented the increase expression of NOX4, NOX2 and NF-κB in the high glucose -stimulated H9c2 cells and diabetic hearts. Conclusions Our results demonstrate that the cardioprotective effect of polydatin against hyperglycemia-induced myocardial injury is mediated by inhibition of NADPH oxidase and NF-κB activity. The findings may provide a novel understanding the mechanisms of the polydatin to be a potential treatment of diabetic cardiomyopathy.

scholarly journals Evidence for a Specific Diabetic Cardiomyopathy: An Observational Retrospective Echocardiographic Study in 656 Asymptomatic Type 2 Diabetic Patients

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Isabelle Pham ◽  
Emmanuel Cosson ◽  
Minh Tuan Nguyen ◽  
Isabela Banu ◽  
Isabelle Genevois ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Silent Myocardial Ischemia ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Asymptomatic Patients ◽  
Artery Disease ◽  
Type 2 Diabetic

Aim. Our aim was to assess the prevalence of subclinical diabetic cardiomyopathy, occurring among diabetic patients without hypertension or coronary artery disease (CAD).Methods. 656 asymptomatic patients with type 2 diabetes for 14 ± 8 years (359 men, 59.7 ± 8.7 years old, HbA1c 8.7 ± 2.1%) and at least one cardiovascular risk factor had a cardiac echography at rest, a stress cardiac scintigraphy to screen for silent myocardial ischemia (SMI), and, in case of SMI, a coronary angiography to screen for silent CAD.Results. SMI was diagnosed in 206 patients, and 71 of them had CAD. In the 157 patients without hypertension or CAD, left ventricular hypertrophy (LVH: 24.1%) was the most frequent abnormality, followed by left ventricular dilation (8.6%), hypokinesia (5.3%), and systolic dysfunction (3.8%). SMI was independently associated with hypokinesia (odds ratio 14.7 [2.7–81.7],p<0.01) and systolic dysfunction (OR 114.6 [1.7–7907],p<0.01), while HbA1c (OR 1.9 [1.1–3.2],p<0.05) and body mass index (OR 1.6 [1.1–2.4],p<0.05) were associated with systolic dysfunction. LVH was more prevalent among hypertensive patients and hypokinesia in the patients with CAD.Conclusion. In asymptomatic type 2 diabetic patients, diabetic cardiomyopathy is highly prevalent and is predominantly characterized by LVH. SMI, obesity, and poor glycemic control contribute to structural and functional LV abnormalities.

scholarly journals Left Ventricular Diastolic Dysfunction in Type 2 Diabetes—Progress and Perspectives

Diagnostics ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 121 ◽  
Author(s):  
Elena-Daniela Grigorescu ◽  
Cristina-Mihaela Lacatusu ◽  
Mariana Floria ◽  
Bogdan-Mircea Mihai ◽  
Ioana Cretu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diastolic Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Cardiovascular Events ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Screening Programs ◽  
Ventricular Diastolic Dysfunction

In-depth understanding of early cardiovascular manifestations in diabetes is high on international research and prevention agendas given that cardiovascular events are the leading cause of death for diabetic patients. Our aim was to review recent developments in the echocardiographic assessment of left ventricular diastolic dysfunction (LVDD) as a telltale pre-clinical disturbance preceding diabetic cardiomyopathy. We analyzed papers in which patients had been comprehensively assessed echocardiographically according to the latest LVDD guidelines (2016), and those affording comparisons with previous, widely used recommendations (2009). We found that the updated algorithm for LVDD is more effective in predicting adverse cardiovascular events in patients with established LVDD, and less specific in grading other patients (labelled “indeterminate”). This may prove instrumental for recruiting “indeterminate” LVDD cases among patients with type 2 diabetes mellitus (T2DM) in future screening programs. As an interesting consideration, the elevated values of the index E/e’ can point to early diastolic impairment, foretelling diabetic cardiomyopathy. Identifying subclinical signs early makes clinical sense, but the complex nature of T2DM calls for further research. Specifically, longitudinal studies on rigorously selected cohorts of diabetic patients are needed to better understand and predict the subtle, slow onset of cardiac manifestations with T2DM as a complicating backdrop.

scholarly journals Skeletal changes in type-2 diabetic Goto-Kakizaki rats

2003 ◽  
Vol 178 (1) ◽  
pp. 111-116 ◽  
Author(s):  
T Ahmad ◽  
C Ohlsson ◽  
M Saaf ◽  
CG Ostenson ◽  
A Kreicbergs
Keyword(s):  
Type 2 Diabetes ◽  
Trabecular Bone ◽  
Bending Strength ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Mineral Density ◽  
Trabecular Bone Mineral Density ◽  
Cross Sectional ◽  
Vertebral Bodies

We characterized appendicular and axial bones in rats with type-2 diabetes in five female Goto-Kakizaki (GK) rats, a strain developed from the Wistar rat showing spontaneous type-2 diabetes, and five age- and sex-matched non-diabetic Wistar rats. The humerus, tibia, metatarsals and vertebral bodies were analysed by peripheral quantitative computerized tomography (pQCT). In diabetic rats, the height of the vertebral bodies and length of the humerus were decreased while the length of the metatarsals was increased. A decreased cross-sectional area was found in the vertebral end-plate region and the tibial metaphysis. Notably, the diaphysis in all long bones showed expansion of periosteal and endosteal circumference. In tibia this resulted in increased cortical thickness, whereas in humerus and metatarsal it was unchanged. Areal moment of inertia was increased in all diaphyses suggesting greater bending strength. The most conspicuous finding in diabetic rats pertained to trabecular osteopenia. Thus, trabecular bone mineral density was significantly reduced in all bones examined, by 33-53%. Our pQCT study of axial and appendicular bones suggests that the typical feature of diabetic osteopathy in the GK rat is loss of trabecular bone and expansion of the diaphysis. The loss of metaphyseal trabecular bone if also present in diabetic patients may prove to underlie the susceptibility to periarticular fracture and Charcot arthropathy. The findings suggest that the risk of fracture in diabetes varies according to the specific sub-regions of a bone. The approach described may prove to be useful in the early detection of osteopathy in diabetic patients who may be amenable to preventive treatment.

scholarly journals The vascular smooth muscle cell: a therapeutic target in Type 2 diabetes?

2013 ◽  
Vol 125 (4) ◽  
pp. 167-182 ◽  
Author(s):  
Karen E. Porter ◽  
Kirsten Riches
Keyword(s):  
Type 2 Diabetes ◽  
Smooth Muscle ◽  
Cardiovascular Risk ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Experimental Studies ◽  
Metabolic Memory ◽  
Diabetic Patients ◽  
Metabolic Disturbances

The rising epidemic of T2DM (Type 2 diabetes mellitus) worldwide is of significant concern. The inherently silent nature of the disease in its early stages precludes early detection; hence cardiovascular disease is often established by the time diabetes is diagnosed. This increased cardiovascular risk leads to significant morbidity and mortality in these individuals. Progressive development of complications as a result of previous exposure to metabolic disturbances appears to leave a long-lasting impression on cells of the vasculature that is not easily reversed and is termed ‘metabolic memory’. SMCs (smooth muscle cells) of blood vessel walls, through their inherent ability to switch between a contractile quiescent phenotype and an active secretory state, maintain vascular homoeostasis in health and development. This plasticity also confers SMCs with the essential capacity to adapt and remodel in pathological states. Emerging clinical and experimental studies propose that SMCs in diabetes may be functionally impaired and thus contribute to the increased incidence of macrovascular complications. Although this idea has general support, the underlying molecular mechanisms are currently unknown and hence are the subject of intense research. The aim of the present review is to explore and evaluate the current literature relating to the problem of vascular disease in T2DM and to discuss the critical role of SMCs in vascular remodelling. Possibilities for therapeutic strategies specifically at the level of T2DM SMCs, including recent novel advances in the areas of microRNAs and epigenetics, will be evaluated. Since restoring glucose control in diabetic patients has limited effect in ameliorating their cardiovascular risk, discovering alternative strategies that restrict or reverse disease progression is vital. Current research in this area will be discussed.

scholarly journals Gene therapy targeting cardiac phosphoinositide 3-kinase (p110α) attenuates cardiac remodeling in type 2 diabetes

2020 ◽  
Vol 318 (4) ◽  
pp. H840-H852 ◽  
Author(s):  
Darnel Prakoso ◽  
Miles J. De Blasio ◽  
Mitchel Tate ◽  
Helen Kiriazis ◽  
Daniel G. Donner ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Gene Therapy ◽  
Cause Of Death ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Remodeling ◽  
Systolic Dysfunction ◽  
Phosphoinositide 3 Kinase ◽  
Fractional Shortening

Diabetic cardiomyopathy is a distinct form of heart disease that represents a major cause of death and disability in diabetic patients, particularly, the more prevalent type 2 diabetes patient population. In the current study, we investigated whether administration of recombinant adeno-associated viral vectors carrying a constitutively active phosphoinositide 3-kinase (PI3K)(p110α) construct (rAAV6-caPI3K) at a clinically relevant time point attenuates diabetic cardiomyopathy in a preclinical type 2 diabetes (T2D) model. T2D was induced by a combination of a high-fat diet (42% energy intake from lipid) and low-dose streptozotocin (three consecutive intraperitoneal injections of 55 mg/kg body wt), and confirmed by increased body weight, mild hyperglycemia, and impaired glucose tolerance (all P < 0.05 vs. nondiabetic mice). After 18 wk of untreated diabetes, impaired left ventricular (LV) systolic dysfunction was evident, as confirmed by reduced fractional shortening and velocity of circumferential fiber shortening (Vcfc, all P < 0.01 vs. baseline measurement). A single tail vein injection of rAAV6-caPI3K gene therapy (2×1011vector genomes) was then administered. Mice were followed for an additional 8 wk before end point. A single injection of cardiac targeted rAAV6-caPI3K attenuated diabetes-induced cardiac remodeling by limiting cardiac fibrosis (reduced interstitial and perivascular collagen deposition, P < 0.01 vs. T2D mice) and cardiomyocyte hypertrophy (reduced cardiomyocyte size and Nppa gene expression, P < 0.001 and P < 0.05 vs. T2D mice, respectively). The diabetes-induced LV systolic dysfunction was reversed with rAAV6-caPI3K, as demonstrated by improved fractional shortening and velocity of circumferential fiber shortening (all P < 0.05 vs pre-AAV measurement). This cardioprotection occurred in combination with reduced LV reactive oxygen species ( P < 0.05 vs. T2D mice) and an associated decrease in markers of endoplasmic reticulum stress (reduced Grp94 and Chop, all P < 0.05 vs. T2D mice). Together, our findings demonstrate that a cardiac-selective increase in PI3K(p110α), via rAAV6-caPI3K, attenuates T2D-induced diabetic cardiomyopathy, providing proof of concept for potential translation to the clinic. NEW & NOTEWORTHY Diabetes remains a major cause of death and disability worldwide (and its resultant heart failure burden), despite current care. The lack of existing management of heart failure in the context of the poorer prognosis of concomitant diabetes represents an unmet clinical need. In the present study, we now demonstrate that delayed intervention with PI3K gene therapy (rAAV6-caPI3K), administered as a single dose in mice with preexisting type 2 diabetes, attenuates several characteristics of diabetic cardiomyopathy, including diabetes-induced impairments in cardiac remodeling, oxidative stress, and function. Our discovery here contributes to the previous body of work, suggesting the cardioprotective effects of PI3K(p110α) could be a novel therapeutic approach to reduce the progression to heart failure and death in diabetes-affected patients.

Abstract 842: Potential Role of MicroRNAs in the Pathogenesis of Diabetic Cardiomyopathy

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ioannis Karakikes ◽  
Andrew Feber ◽  
Tony E Godfrey ◽  
Roger J Hajjar ◽  
Djamel Lebeche
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Diabetic Cardiomyopathy ◽  
Myocardial Dysfunction ◽  
Microarray Platform ◽  
Calcium Handling ◽  
Diabetic Patients ◽  
Rna Molecules

Cardiac dysfunction is a common and important manifestation of diabetes mellitus and accounts for much of the increased mortality in diabetic patients. Recent studies have uncovered key roles for a family of newly discovered small non-coding regulatory RNA molecules, known as microRNAs (miRNAs), in the control of diverse aspects of cardiac function and dysfunction. However, it remains to be shown whether the expression of miRNAs is altered in the heart in response to diabetes and accounts for the pathogenesis of the disease. We have determined the expression profile of miRNAs in the heart of a rat model of type 2 diabetes using a custom Affymetrix microarray platform in order to gain a better understanding of their possible involvement in diabetic cardiomyopathy. We Identified 17 miRNAs that are differentially regulated during diabetic cardiomyopathy, suggesting that they might function as modulators of this condition. Interestingly, most of the identified miRNAs were similarly dysregulated in type 2 diabetic failing human hearts. Since type 2 diabetes is associated with insulin resistance, we further investigated the functional significance of these miRNAs by over-expression using synthetic miRNA mimics in vitro . Overexpression of a single miRNA (mir-152), which was up-regulated in diabetic cardiomyopathy, inhibited insulin-stimulated glucose uptake and induced cardiac hypertrophy in rat neonatal myocytes. Additionally, mir-152 significantly increased the Phospholamban/Serca2a ratio, suggesting abnormal calcium handling. Our results suggest that specific miRNAs play important roles in myocardial dysfunction associated with insulin resistance and may provide novel therapeutic approaches for the management of diabetes-induced cardiomyopathy.

scholarly journals Probiotics Ameliorate Pioglitazone-associated Bone Loss in Diabetic Rats

2020 ◽  
Author(s):  
Ahmad Gholami ◽  
Mohammad Hossein Dabbaghmanesh ◽  
Younes Ghasemi ◽  
Pedram Talezadeh ◽  
Farhad Koohpeyma ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Bone Loss ◽  
Lactobacillus Reuteri ◽  
Diabetic Rats ◽  
Urinary Calcium ◽  
Diabetic Patients ◽  
Protective Effects

Abstract Background: Pioglitazone as a PPAR-g agonist are used for management of type 2 diabetes mellitus. Nevertheless, evidence showed that the therapeutic modulation of PPARg activity using Pioglitazone may be linked with bone mass reduction and fracture risk in type 2 diabetes mellitus patients. The objective of the current research was to inspect the preventive role of some types of probiotic strains including (Lactobacillus acidophilus, Lactobacillus reuteri, Lactobacillus casei, Bifidiobacterum longum and Bacillus coagulans) against pioglitazone-induced bone loss.Methods: Streptozotocin (60 mg/kg) was administered for diabetes induction. Diabetic rats were fed orally with pioglitazone (300 mg/kg) and probiotics (1×109 CFU/ml/day) alone and in combination of both for 4 weeks. Dual energy X-ray absorptiometry (DEXA) were used to asses BMD, BMC and area of the femur, spine and tibia at the experiment termination. Serum glucose, serum calcium, alkaline phosphatase, phosphorus, BUN, Creatinine, and urine calcium were also analyzed. Results: Administration of pioglitazone and probiotics alone and in combination significantly improved elevated blood glucose. Pioglitazone treatment significantly increased urinary calcium and BUN, and decreased ALP and creatinine. Co-treatment of probiotics with pioglitazone significantly decreased urinary calcium, creatinine and ALP. Pioglitazone showed detrimental effects on femur-BMD whereas treatment with probiotics remarkably ameliorated these effects. Among the tested probiotics Bifidiobacterum longum displayed the best protective effects on pioglitazone-induced bone loss in diabetic rats.Conclusion:This study suggests probiotic supplementation in diabetic patients on pioglitazone regime could be considering as a good strategy to ameliorate bone loss induced by pioglitazone.

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