scholarly journals In Vivo Hypoglycemic Effect of Kigelia africana (Lam): Studies With Alloxan-Induced Diabetic Mice

2018 ◽  
Vol 23 ◽  
pp. 2515690X1876872 ◽  
Author(s):  
Stephen M. Njogu ◽  
Wycliffe M. Arika ◽  
Alex K. Machocho ◽  
Joseph J. N. Ngeranwa ◽  
Eliud N. M. Njagi
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Ethyl Acetate ◽  
Leaf Extract ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Physiological Saline ◽  
Diabetic Control ◽  
Type I ◽  
Diabetic Mice

The claims by the traditional herbal medicine practitioners that Kigelia africana has bioactivity against several diseases, including diabetes mellitus, were investigated in this study. Type I diabetes mellitus was induced in mice by intraperitoneal administration of alloxan monohydrate followed by treatment with the therapeutic doses of the aqueous and ethyl acetate leaf extract of K africana to the experimentally diabetic mice. The treatment effects were compared with the normal control, diabetic control, and diabetic control rats treated with a standard antidiabetic drugs (insulin administered intraperitoneally at 1 IU/kg body weight in 0.1 mL physiological saline or glibenclamide administered orally at 3 mg/kg body weight in 0.1 mL physiological saline). Phytochemical composition of the leaf extract was assessed using standard procedures and mineral elements assessed using atomic absorption spectrophotometry and total reflection X-ray fluorescence system. Oral and intraperitoneal administration of the aqueous and ethyl acetate leaf extract caused a statistically significant dose-independent reduction in plasma glucose level in alloxan-induced diabetic mice. The observed hypoglycemic activity of this plant extract could be attributed to the observed phytochemicals and trace elements, which have been associated with exhibiting antidiabetic properties. Therefore, the data appear to support the hypoglycemic effects of K africana validating its folkloric usage.

scholarly journals In vivo antidiabetic activity of aqueous and ethyl acetate leaf extract of Senna singuena (Delile) in alloxan induced diabetic mice

2017 ◽  
Vol 6 (2) ◽  
pp. 84-92
Author(s):  
Njogu M. Stephen ◽  
◽  
Arika M. Wycliffe ◽  
Machocho K. Alex ◽  
Ngeranwa J.N. Joseph ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Plant Extract ◽  
Leaf Extract ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Scientific Data ◽  
Hypoglycemic Activity ◽  
Antidiabetic Activity ◽  
Type I ◽  
Diabetic Mice

The folkloric claims that Senna singuena confers antidiabetic effect to prescribed patients has received long term clinical application accompanied by limited scientific data in support of such claims. This study aimed at bioscreening for hypoglycemic activity of the aqueous and organic fractions of S. singuena in alloxan induced diabetic mice. Type I diabetes mellitus was induced in mice by intraperitoneal administration of alloxan monohydrate followed by graded doses of the aqueous and ethyl acetate leaf extract administered to the experimentally diabetic mice following an overnight fast. The composition of the various phytochemicals of the plant extract was quantitatively assessed using standard procedures. Oral and intraperitoneal administration of the aqueous and ethyl acetate leaf extract caused a significant reduction in plasma glucose level in a dose independent manner in both fractions. The hypoglycemic activity could be attributed to phytoconstituents found in the plant extract. The generated data supports the folkloric claims associating S. singuena with hypoglycemic effects. However, there is need for further studies on this plant to investigate the mechanism of its activity and determine its safety profiles in order to explore possibilities of developing a new antidiabetic drug.

scholarly journals Contribution of Trem2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
Xin Chen ◽  
Yue Le ◽  
Wan-you He ◽  
Jian He ◽  
Yun-hua Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes. Methods Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN. Conclusions TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals Contribution of TREM2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
xin chen ◽  
Yue Le ◽  
Si-qi Tang ◽  
Wan-you He ◽  
Jian He ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background: Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes.Methods：Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results：We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN.Conclusions: TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals Thyroid auto immune antibodies in children with Type-I Diabetes mellitus in relation to diabetes control

2019 ◽  
Vol 35 (4) ◽  
Author(s):  
Muneera Fadhil Ridha ◽  
Munib Ahmed Al Zubaidi
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Glycemic Control ◽  
Type I Diabetes ◽  
Thyroid Autoimmunity ◽  
Diabetic Control ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Thyroid Antibodies

Background & Objective: As an autoimmune disease, Type-1 diabetes mellitus (DM) may be associated with other autoimmune disorders, the presence of thyroid antibodies could be negatively impact the diabetic control. Our objective was to investigate thyroid autoimmunity in a cohort of children and adolescents with Type-1 diabetes and the Influence of the presence of thyroid autoimmune abnormalities on the control of diabetes in group of Iraqi pediatric patients with Type-I D.M. Methods: This study was conducted at the Medical City Complex, Children Welfare Hospital, Baghdad, Iraq. This study was carried out from the first of January 2016 till the end of September 2017. Data were analyzed from 150 patients with Type-1 diabetes, aged 1–18 years who were treated and are coming for regular follow up in the diabetic clinic. Thyroid functions tests, Antibodies to thyroglobulin (anti-TG) and thyroperoxidase (anti-TPO) were measured, documented and correlated with diabetic control according to glycated haemoglobin (HbA1c) level. Results: In the total of 150 patients, positive Antibodies to thyroglobulin (anti TG) were more in ≤3 years duration group of Diabetes mellitus( DM) and negative anti TG was less in the >3 years duration of DM group with statistically significant results (p=0.043), Regarding the distribution of thyroid antibodies (AB) according to HbA1c group, there was progressive positive anti thyroperoxidase (anti TPO) titer with glycemic status, good glycemic control had the lowest positive anti TPO titer and poor glycemic control group had the highest positive anti TPO titer and the result was statistically significant (p=0.048). Conclusions: Thyroid autoimmunity may be associated with poor diabetic control and elevated TSH levels, indicating subclinical hypothyroidism that my affect the diabetic control. doi: https://doi.org/10.12669/pjms.35.4.192 How to cite this:Ridha MF, Al-Zubaidi MA. Thyroid auto immune antibodies in children with type I Diabetes mellitus in relation to diabetes control. Pak J Med Sci. 2019;35(4):---------. doi: https://doi.org/10.12669/pjms.35.4.192 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

scholarly journals Type I Diabetes Mellitus Increases the Cardiovascular Complications of Influenza Virus Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Jane E. Sinclair ◽  
Conor J. Bloxham ◽  
Han Chiu ◽  
Keng Yih Chew ◽  
Jake Russell ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Virus Infection ◽  
Type I Diabetes ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Cardiac Complications ◽  
Type I ◽  
Diabetic Mice ◽  
Infected Control ◽  
Creatine Kinase Mb

People with diabetes mellitus are susceptible to both cardiovascular disease and severe influenza A virus infection. We hypothesized that diabetes also increases risks of influenza-associated cardiac complications. A murine type 1 (streptozotocin-induced) diabetes model was employed to investigate influenza-induced cardiac distress. Lung histopathology and viral titres revealed no difference in respiratory severity between infected control and diabetic mice. However, compared with infected control mice, infected diabetic mice had increased serum cardiac troponin I and creatine-kinase MB, left ventricular structural changes and right ventricular functional alterations, providing the first experimental evidence of type I diabetes increasing risks of influenza-induced cardiovascular complications.

Hepatoprotective effect of seabuckthorn leaf extract in streptozotocin induced diabetes mellitus in Wistar rats

2018 ◽  
Author(s):  
P. Khajuria ◽  
P. Raghuwanshi ◽  
A. Rastogi ◽  
A. L. Koul ◽  
R. Zargar ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Wistar Rats ◽  
Leaf Extract ◽  
Diabetic Control ◽  
Negative Control ◽  
Diabetic Rats ◽  
Hepatoprotective Effect ◽  
Male Wistar Rats ◽  
Streptozotocin Induced Diabetes

Study was conducted to evaluate the hepatoprotective effects of Seabuckthorn leaf extract (SLE) supplementation on serum enzymatic levels in streptozotocin (STZ) induced diabetes mellitus in Wistar rats. Thirty-two adult male Wistar rats were divided into four groups namely CON (negative control), SCO (Seabuckthorn control), DCO (Diabetic control), and DSL (Diabetic seabuckthorn treatment group). Diabetes mellitus was induced by single intra peritoneal injection of STZ @ 50 mg/kg body weight in DCO and DSL group of rats. SLE was administered orally @ 100mg/kg body weight for 40 days to SCO and DSL groups. CON served as the negative control. Blood samples were collected from experimental animals on zero, 20th, and 40th days of trial to study liver specific serum enzyme profile viz aspartate amino transaminase (AST), alanine amino transaminase (ALT), alkaline phosphatase (ALP) and acid phosphatase (ACP). Significantly (P less than 0.01) higher levels of all the enzymes studied were observed in experimentally induced diabetic rats in comparison to normal rats. However, in SLE treated diabetic rats (DSL group), significant (P less than 0.01) improvement was observed in all the above enzymes. It may be concluded that SLE exerts hepatoprotective effect in STZ induce Diabetes mellitus in Wistar rats.

Human Amnion-Isolated Cells Normalize Blood Glucose in Streptozotocin-Induced Diabetic Mice

2003 ◽  
Vol 12 (5) ◽  
pp. 545-552 ◽  
Author(s):  
Jun Ping Wei ◽  
Tian Shu Zhang ◽  
Shigeyuki Kawa ◽  
Toru Aizawa ◽  
Masao Ota ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Type I Diabetes ◽  
Cell Mass ◽  
Mouse Tissue ◽  
Fetal Membrane ◽  
Type I ◽  
Diabetic Mice ◽  
Human Specific

Whole pancreas or β-cell transplantation has opened the way for the treatment of advanced stage of diabetes mellitus. However, it is always limited by the scarcity of transplantation materials. The amniotic membrane is part of the fetal membrane and is composed of amniotic epithelium (HAE) and mesenchymal (HAM) cells that are derived from the inner cell mass in the blastocyst. Thus, HAE and HAM cells may have the potential to differentiate into various organs. The aim of our study was to assess the possibility of HAE cells differentiating into insulin-producing cells. In vitro, HAE cells stimulated with nicotinamide induced insulin mRNA in the culture cells. In vivo, HAE cells were capable of normalizing the blood glucose level of diabetic mice after several weeks of implantation into streptozotocin-induced diabetic mice. The distribution of human cells and human insulin secretion in mouse tissue studied by immunohistochemistry for anti-human-specific β-2-microglobulin and anti-human-specific insulin shows the same location in mouse tissue. These studies suggest that HAE cells have the potential to differentiate into β-cells in vivo, and hence that HAE cells have therapeutic potential for the treatment of type I diabetes mellitus.

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