scholarly journals Nutrigenomics in Regulating the Expression of Genes Related to Type 2 Diabetes Mellitus

2021 ◽  
Vol 12 ◽  
Author(s):  
Karoline Felisbino ◽  
Juliano Gomes Granzotti ◽  
Larissa Bello-Santos ◽  
Izonete Cristina Guiloski
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Bioactive Compounds ◽  
Cell Mass ◽  
Expression Of Genes ◽  
Human Genes ◽  
Regular Consumption ◽  
Positive Results

Nutrigenomics is the study of the gene-nutrient interaction and it indicates that some nutrients, called bioactive compounds, can mold the genetic expression or change the nucleotide chain. Polyphenols are secondary metabolites found in plants that are regularly consumed in functional foods and help prevent or delay the onset of type 2 diabetes mellitus (T2DM) and its complications. This article objected to review studies about the interaction of diet with polyphenols and Mediterranean diet in the expression of human genes related to T2DM. Resveratrol acts as an antioxidant, anti-inflammatory, and increases mitochondrial function. Regular consumption of quercetin resulted in improvement of hypertension and suppression of diabetes-induced vasoconstriction. Genistein also showed positive results in T2DM, such as increased cell mass and improved glucose tolerance and insulin levels. Catechins showed efficiency in inducing genes in triacylglycerol biosynthesis, inhibition of fatty acids and cholesterol, and resulting in their participation in mitigating complications of diabetes. Lastly, curcumin was demonstrated to be a protector of the pancreatic islets against streptozotocin-induced oxidative stress. Growing evidence suggest that bioactive compounds such as polyphenols have an important role in T2DM and the prevention and treatment of its complication, as they cause activation or inhibition of related genes.

scholarly journals Incretin-Based Therapies in Type 2 Diabetes Mellitus

2008 ◽  
Vol 93 (10) ◽  
pp. 3703-3716 ◽  
Author(s):  
Chee W. Chia ◽  
Josephine M. Egan
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Weight Loss ◽  
Type 2 Diabetes Mellitus ◽  
Evidence Synthesis ◽  
Glycosylated Hemoglobin ◽  
Cell Mass ◽  
New Drugs ◽  
Medline Search

Context: Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide are incretins secreted from enteroendocrine cells postprandially in part to regulate glucose homeostasis. Dysregulation of these hormones is evident in type 2 diabetes mellitus (T2DM). Two new drugs, exenatide (GLP-1 mimetic) and sitagliptin [dipeptidyl peptidase (DPP) 4 inhibitor], have been approved by regulatory agencies for treating T2DM. Liraglutide (GLP-1 mimetic) and vildagliptin (DPP 4 inhibitor) are expected to arrive on the market soon. Evidence Acquisition: The background of incretin-based therapy and selected clinical trials of these four drugs are reviewed. A MEDLINE search was conducted for published articles using the key words incretin, glucose-dependent insulinotropic polypeptide, GLP-1, exendin-4, exenatide, DPP 4, liraglutide, sitagliptin, and vildagliptin. Evidence Synthesis: Exenatide and liraglutide are injection based. Three-year follow-up data on exenatide showed a sustained weight loss and glycosylated hemoglobin (HbA1c) reduction of 1%. Nausea and vomiting are common. Results from phase 3 studies are pending on liraglutide. Sitagliptin and vildagliptin are orally active. In 24-wk studies, sitagliptin reduces HbA1c by 0.6–0.8% as monotherapy, 1.8% as initial combination therapy with metformin, and 0.7% as add-on therapy to metformin. Vildagliptin monotherapy lowered HbA1c by 1.0–1.4% after 24 wk. Their major side effects are urinary tract and nasopharyngeal infections and headaches. Exenatide and liraglutide cause weight loss, whereas sitagliptin and vildagliptin do not. Conclusions: The availability of GLP-1 mimetics and DPP 4 inhibitors has increased our armamentarium for treating T2DM. Unresolved issues such as the effects of GLP-1 mimetics and DPP 4 inhibitors on β-cell mass, the mechanism by which GLP-1 mimetics lowers glucagon levels, and exactly how DPP 4 inhibitors lead to a decline in plasma glucose levels without an increase in insulin secretion, need further research.

Reduced body cell mass in type 2 diabetes mellitus: reversal with a diabetes-specific nutritional formula

2010 ◽  
Vol 3 (2) ◽  
pp. 133-136 ◽  
Author(s):  
Patrizio Tatti ◽  
Patrizia di Mauro ◽  
Marisa Neri ◽  
Giuseppe Pipicelli ◽  
Felice Strollo
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Mass ◽  
Body Cell Mass ◽  
Body Cell ◽  
Reduced Body

Reduced body cell mass in type 2 diabetes mellitus: reversal with a diabetes-specific nutritional formula

2010 ◽  
Vol 3 (2) ◽  
pp. 133-136 ◽  
Author(s):  
Patrizio Tatti ◽  
Patrizia di Mauro ◽  
Marisa Neri ◽  
Giuseppe Pipicelli ◽  
Felice Strollo
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Mass ◽  
Body Cell Mass ◽  
Body Cell ◽  
Reduced Body

scholarly journals XOMA 052, an Anti-IL-1β Monoclonal Antibody, Improves Glucose Control and β-Cell Function in the Diet-Induced Obesity Mouse Model

2010 ◽  
Vol 31 (2) ◽  
pp. 261-261
Author(s):  
Alexander M. Owyang ◽  
Kathrin Maedler ◽  
Lisa Gross ◽  
Johnny Yin ◽  
Lin Esposito ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Monoclonal Antibody ◽  
Type 2 Diabetes Mellitus ◽  
Cell Function ◽  
Cell Mass ◽  
Β Cell ◽  
Diet Induced Obesity ◽  
Β Cell Function

ABSTRACT Recent evidence suggests that IL-1β-mediated glucotoxicity plays a critical role in type 2 diabetes mellitus. Although previous work has shown that inhibiting IL-1β can lead to improvements in glucose control and β-cell function, we hypothesized that more efficient targeting of IL-1β with a novel monoclonal antibody, XOMA 052, would reveal an effect on additional parameters affecting metabolic disease. In the diet-induced obesity model, XOMA 052 was administered to mice fed either normal or high-fat diet (HFD) for up to 19 wk. XOMA 052 was administered as a prophylactic treatment or as a therapy. Mice were analyzed for glucose tolerance, insulin tolerance, insulin secretion, and lipid profile. In addition, the pancreata were analyzed for β-cell apoptosis, proliferation, and β-cell mass. Mice on HFD exhibited elevated glucose and glycated hemoglobin levels, impaired glucose tolerance and insulin secretion, and elevated lipid profile, which were prevented by XOMA 052. XOMA 052 also reduced β-cell apoptosis and increased β-cell proliferation. XOMA 052 maintained the HFDinduced compensatory increase in β-cell mass, while also preventing the loss in β-cell mass seen with extended HFD feeding. Analysis of fasting insulin and glucose levels suggests that XOMA 052 prevented HFD-induced insulin resistance. These studies provide new evidence that targeting IL-1β in vivo could improve insulin sensitivity and lead to β-cell sparing. This is in addition to previously reported benefits on glycemic control. Taken together, the data presented suggest that XOMA 052 could be effective for treating many aspects of type 2 diabetes mellitus.

scholarly journals Verapamil can be used as a Type 2 Diabetes Mellitus Saviour and Stopping the need for Insulin in Uncontrolled Type 2 Diabetes Mellitus

2021 ◽  
pp. 1-8
Author(s):  
Mahmoud Younis ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Beta Cell ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Interacting Protein ◽  
Significant Difference ◽  
And Function

Introduction: Diabetes mellitus is not just a disease as it is already known, the matter is more complicated, and it is considered as an assembly of metabolic defects with end result of hyperglycemia.verapamil can decrease the expression of thioredoxin-interacting protein (TXNIP), which is recognized as an important factor in pancreatic beta cells.verapamil could enhance beta cell mass and function. Materials and Methods: 160 type 2 diabetes patients in 2 parallel groups. Results: show statistically significant difference in favour of verapamil in increasing c-peptide levels and decreasing hba1c levels. Conclusion: Verapamil could be used as a type 2 diabetes saviour by increasing beta cell mass and function.

scholarly journals Insulin: The Friend and the Foe in the Development of Type 2 Diabetes Mellitus

2020 ◽  
Vol 21 (5) ◽  
pp. 1770
Author(s):  
Nadia Rachdaoui
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Secretion ◽  
Cell Mass ◽  
Β Cells ◽  
Β Cell ◽  
Peripheral Insulin Resistance

Insulin, a hormone produced by pancreatic β-cells, has a primary function of maintaining glucose homeostasis. Deficiencies in β-cell insulin secretion result in the development of type 1 and type 2 diabetes, metabolic disorders characterized by high levels of blood glucose. Type 2 diabetes mellitus (T2DM) is characterized by the presence of peripheral insulin resistance in tissues such as skeletal muscle, adipose tissue and liver and develops when β-cells fail to compensate for the peripheral insulin resistance. Insulin resistance triggers a rise in insulin demand and leads to β-cell compensation by increasing both β-cell mass and insulin secretion and leads to the development of hyperinsulinemia. In a vicious cycle, hyperinsulinemia exacerbates the metabolic dysregulations that lead to β-cell failure and the development of T2DM. Insulin and IGF-1 signaling pathways play critical roles in maintaining the differentiated phenotype of β-cells. The autocrine actions of secreted insulin on β-cells is still controversial; work by us and others has shown positive and negative actions by insulin on β-cells. We discuss findings that support the concept of an autocrine action of secreted insulin on β-cells. The hypothesis of whether, during the development of T2DM, secreted insulin initially acts as a friend and contributes to β-cell compensation and then, at a later stage, becomes a foe and contributes to β-cell decompensation will be discussed.

scholarly journals Administration of mulberry leaves maintains pancreatic β-cell mass in obese/type 2 diabetes mellitus mouse model

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Patlada Suthamwong ◽  
Manabu Minami ◽  
Toshiaki Okada ◽  
Nonomi Shiwaku ◽  
Mai Uesugi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mouse Model ◽  
Cell Mass ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Mulberry Leaves
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