Beneficial effects of antioxidants in diabetes: possible protection of pancreatic beta-cells against glucose toxicity

Background: Diabetes mellitus (DM) is a chronic disease, progressing due to inadequate secretion of insulin by pancreas. Salvia officinalis (SVO) has anti-inflammatory and anti-oxidative potentials, which may be beneficial in regulating underlying causes of DM. Objectives: In this study, we aimed to estimate the protective effects of SVO against Streptozotocin (STZ)-induced pancreatic injury in rat models of DM. Methods: Forty-eight male Sprague-Dawley rats were randomly divided into four groups (n = 12); C1: normal group with no treatment, C2: diabetic group with no treatment, E1: diabetic group treated with 200 mg/kg of the SVO extract, and E2: diabetic group treated with 400 mg/kg of the SVO extract. All groups received a single dose of STZ on day 7 except C1. Pancreas volume, shrinkage, volume densities of the islets, numerical densities, and volume of the beta cells were measured using stereological methods. Results: Blood sugar (BS) levels were significantly lower in SVO-treated groups comparing to C2 group. Also, volume densities and total number of islets and beta cells in E1 and E2 groups were higher than C2 (P < 0.05), but lower than C1 (P < 0.05). Volume densities of the islets and beta cells, and total number of beta cells in E1, and volume densities of the islets and beta cells in E2 groups were considerably higher than C2 group (P < 0.05). Conclusions: Our result showed the beneficial effects of SVO extract regarding pancreatic damage. We concluded that SVO might be prescribed as a therapeutic food supplement for patients with diabetes.

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Metformin’s Therapeutic Action in the Treatment of Diabetes Does Not Involve Inhibition of Mitochondrial Glycerol Phosphate Dehydrogenase

10.2337/figshare.14394359 ◽

2021 ◽

Author(s):

Michael J. MacDonald ◽

Israr-ul H. Ansari ◽

Melissa J. Longacre ◽

Scott W. Stoker

Keyword(s):

Adverse Effects ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Glycerol Phosphate ◽

Beneficial Effects ◽

Insulin Cells ◽

Cast Doubt ◽

Redox Shuttle ◽

Treatment Of Diabetes ◽

Glycerol Phosphate Dehydrogenase

Mitochondrial glycerol phosphate dehydrogenase (mGPD) is the rate-limiting enzyme of the glycerol phosphate redox shuttle. It was recently claimed that metformin, a first line drug used for the treatment of type 2 diabetes, inhibits liver mGPD 30-50% suppressing gluconeogenesis through a redox mechanism. Various factors cast doubt on this idea. Total body100% knockout of mGPD in mice has adverse effects in several tissues where mGPD is high, but has little or no effect in liver where mGPD is the lowest of ten tissues. Metformin has beneficial effects in humans in tissues with high levels of mGPD such as pancreatic beta cells where mGPD is much higher than in liver. Insulin secretion in mGPD knockout mouse beta cells is normal because, like liver, beta cells possess the malate aspartate redox shuttle that’s redox action is redundant to the glycerol phosphate shuttle. For these and other reasons we used four different enzyme assays to reassess whether metformin inhibited mGPD. Metformin did not inhibit mGPD in homogenates or mitochondria from insulin cells or liver cells. If metformin actually inhibited mGPD, adverse effects in tissues where the level of mGPD is much higher than in liver could prevent metformin’s use as a diabetes medicine.

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Metformin’s Therapeutic Action in the Treatment of Diabetes Does Not Involve Inhibition of Mitochondrial Glycerol Phosphate Dehydrogenase

10.2337/figshare.14394359.v1 ◽

2021 ◽

Author(s):

Michael J. MacDonald ◽

Israr-ul H. Ansari ◽

Melissa J. Longacre ◽

Scott W. Stoker

Keyword(s):

Adverse Effects ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Glycerol Phosphate ◽

Beneficial Effects ◽

Insulin Cells ◽

Cast Doubt ◽

Redox Shuttle ◽

Treatment Of Diabetes ◽

Glycerol Phosphate Dehydrogenase

Mitochondrial glycerol phosphate dehydrogenase (mGPD) is the rate-limiting enzyme of the glycerol phosphate redox shuttle. It was recently claimed that metformin, a first line drug used for the treatment of type 2 diabetes, inhibits liver mGPD 30-50% suppressing gluconeogenesis through a redox mechanism. Various factors cast doubt on this idea. Total body100% knockout of mGPD in mice has adverse effects in several tissues where mGPD is high, but has little or no effect in liver where mGPD is the lowest of ten tissues. Metformin has beneficial effects in humans in tissues with high levels of mGPD such as pancreatic beta cells where mGPD is much higher than in liver. Insulin secretion in mGPD knockout mouse beta cells is normal because, like liver, beta cells possess the malate aspartate redox shuttle that’s redox action is redundant to the glycerol phosphate shuttle. For these and other reasons we used four different enzyme assays to reassess whether metformin inhibited mGPD. Metformin did not inhibit mGPD in homogenates or mitochondria from insulin cells or liver cells. If metformin actually inhibited mGPD, adverse effects in tissues where the level of mGPD is much higher than in liver could prevent metformin’s use as a diabetes medicine.

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Effects of physical exercise on beta cells of the pancreas: a systematic review

Manual Therapy Posturology & Rehabilitation Journal ◽

10.17784/mtprehabjournal.2017.15.544 ◽

2020 ◽

pp. 1-6

Author(s):

Edson Meneses da Silva Filho ◽

Jéssica Andrade de Albuquerque ◽

Roberta de Oliveira Cacho ◽

Rodrigo Pegado de Abreu Freitas

Keyword(s):

Insulin Resistance ◽

Insulin Sensitivity ◽

Physical Exercise ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Randomized Clinical Trials ◽

Qualitative Evaluation ◽

Cochrane Collaboration ◽

Cochrane Library ◽

Beneficial Effects

Background: Diabetes mellitus is a chronic disease that is rising in many parts of the world causing damage to functionality, quality of life and public health system. Objective: Verify the effects of physical exercise on beta cells of the pancreas in diabetic subjects. Methods: The database Cochrane Library via Wiley – CENTRAL, Pubmed, LILACS, SCIELO, Web of Science, Scopus, CINAHL were used to search the articles. The descriptors and synonyms of this topic were used in the search strategy. Controlled randomized clinical trials and quasi-randomized studies, which included in their samples diabetic humans undergone any type of physical exercise were included. The Cochrane collaboration bias risk tool was used to assess the risk of bias. Results: A total of 3.133 articles were initially identified and after reading the titles/abstracts and the full text 6 articles were selected for the qualitative evaluation. Most of the studies showed positive results of physical exercise on pancreatic beta cells, insulin secretion, insulin resistance and insulin sensitivity. The main limitations were the number of studies, few, and their methodological qualities. Conclusions: Physical exercises have beneficial effects on pancreatic beta cells, insulin resistance and insulin sensitivity; however better studies designs, with fewer biases and larger samples are needed so that the results presented do not be overestimated. This review is recorded in the Prospective Register of Systematic Reviews with registration number 42017054213

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Metformin’s Therapeutic Action in the Treatment of Diabetes Does Not Involve Inhibition of Mitochondrial Glycerol Phosphate Dehydrogenase

10.2337/figshare.14394359.v2 ◽

2021 ◽

Author(s):

Michael J. MacDonald ◽

Israr-ul H. Ansari ◽

Melissa J. Longacre ◽

Scott W. Stoker

Keyword(s):

Adverse Effects ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Glycerol Phosphate ◽

Beneficial Effects ◽

Insulin Cells ◽

Cast Doubt ◽

Redox Shuttle ◽

Treatment Of Diabetes ◽

Glycerol Phosphate Dehydrogenase

Mitochondrial glycerol phosphate dehydrogenase (mGPD) is the rate-limiting enzyme of the glycerol phosphate redox shuttle. It was recently claimed that metformin, a first line drug used for the treatment of type 2 diabetes, inhibits liver mGPD 30-50% suppressing gluconeogenesis through a redox mechanism. Various factors cast doubt on this idea. Total body100% knockout of mGPD in mice has adverse effects in several tissues where mGPD is high, but has little or no effect in liver where mGPD is the lowest of ten tissues. Metformin has beneficial effects in humans in tissues with high levels of mGPD such as pancreatic beta cells where mGPD is much higher than in liver. Insulin secretion in mGPD knockout mouse beta cells is normal because, like liver, beta cells possess the malate aspartate redox shuttle that’s redox action is redundant to the glycerol phosphate shuttle. For these and other reasons we used four different enzyme assays to reassess whether metformin inhibited mGPD. Metformin did not inhibit mGPD in homogenates or mitochondria from insulin cells or liver cells. If metformin actually inhibited mGPD, adverse effects in tissues where the level of mGPD is much higher than in liver could prevent metformin’s use as a diabetes medicine.

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