AMP kinase: the missing link between type 2 diabetes and neurodegenerative diseases?

In the population of Poland, as well as in other European countries, an aging process is taking place. It is expected that in Poland in 2050, up to 35% of the population may be seniors. With increasing age, there are numerous changes in the body that necessitate the modification of the current diet. Incorrect diet is a risk factor for many old age diseases, including neurodegenerative diseases, osteoporosis, atherosclerosis, stroke, type 2 diabetes and hypertension. The aim of this study is to review the nutrition recommendations in selected diseases of the elderly. The diet of seniors should provide the right amount of nutrients and be adapted to existing diseases. A proper diet can reduce the risk of complications from senile diseases.

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Curcumin: A small molecule with big functionality against amyloid aggregation in neurodegenerative diseases and type 2 diabetes

BioFactors ◽

10.1002/biof.1735 ◽

2021 ◽

Author(s):

Shabnam Radbakhsh ◽

George E. Barreto ◽

Abigail R. Bland ◽

Amirhossein Sahebkar

Keyword(s):

Type 2 Diabetes ◽

Neurodegenerative Diseases ◽

Small Molecule ◽

Amyloid Aggregation

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Mechanisms Underlying Metformin-Induced Secretion of Glucagon-Like Peptide-1 from the Intestinal L Cell

Endocrinology ◽

10.1210/en.2011-1485 ◽

2011 ◽

Vol 152 (12) ◽

pp. 4610-4619 ◽

Cited By ~ 90

Author(s):

Andrew J. Mulherin ◽

Amy H. Oh ◽

Helena Kim ◽

Anthony Grieco ◽

Lina M. Lauffer ◽

...

Keyword(s):

Type 2 Diabetes ◽

Neural Stimulation ◽

Amp Kinase ◽

Dipeptidylpeptidase Iv ◽

L Cell ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Kinase Phosphorylation ◽

Plasma Activity

Glucagon-like peptide-17-36NH2 (GLP-1) is secreted by the intestinal L cell in response to both nutrient and neural stimulation, resulting in enhanced glucose-dependent insulin secretion. GLP-1 is therefore an attractive therapeutic for the treatment of type 2 diabetes. The antidiabetic drug, metformin, is known to increase circulating GLP-1 levels, although its mechanism of action is unknown. Direct effects of metformin (5–2000 μm) or another AMP kinase activator, aminoimidazole carboxamide ribonucleotide (100–1000 μm) on GLP-1 secretion were assessed in murine human NCI-H716, and rat FRIC L cells. Neither agent stimulated GLP-1 secretion in any model, despite increasing AMP kinase phosphorylation (P < 0.05–0.01). Treatment of rats with metformin (300 mg/kg, per os) or aminoimidazole carboxamide ribonucleotide (250 mg/kg, sc) increased plasma total GLP-1 over 2 h, reaching 37 ± 9 and 29 ± 9 pg/ml (P < 0.001), respectively, compared with basal (7 ± 1 pg/ml). Plasma activity of the GLP-1-degrading enzyme, dipeptidylpeptidase-IV, was not affected by metformin treatment. Pretreatment with the nonspecific muscarinic antagonist, atropine (1 mg/kg, iv), decreased metformin-induced GLP-1 secretion by 55 ± 11% (P < 0.05). Pretreatment with the muscarinic (M) 3 receptor antagonist, 1-1-dimethyl-4-diphenylacetoxypiperidinium iodide (500 μg/kg, iv), also decreased the GLP-1 area under curve, by 48 ± 8% (P < 0.05), whereas the antagonists pirenzepine (M1) and gallamine (M2) had no effect. Furthermore, chronic bilateral subdiaphragmatic vagotomy decreased basal secretion compared with sham-operated animals (7 ± 1 vs. 13 ± 1 pg/ml, P < 0.001) but did not alter the GLP-1 response to metformin. In contrast, pretreatment with the gastrin-releasing peptide antagonist, RC-3095 (100 μg/kg, sc), reduced the GLP-1 response to metformin, by 55 ± 6% (P < 0.01) at 30 min. These studies elucidate the mechanism underlying metformin-induced GLP-1 secretion and highlight the benefits of using metformin with dipeptidylpeptidase-IV inhibitors in patients with type 2 diabetes.

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