scholarly journals Glycolysis intensity and activities of energy metabolism enzymes in the rat brain during repeated exposure to hypoglycemic doses of insulin

1994 ◽  
Vol 40 (5) ◽  
pp. 53-54 ◽  
Author(s):  
P. K. Telushkin ◽  
P. P. Potapov

Renewable conditions of hypoglycemia are a frequent complication in the treatment of diabetes mellitus, determine the clinic of pancreatic insulinomas, are observed in diseases of the kidneys, liver, gastrointestinal tract and alcoholism, leading to the development of posthypoglycemic encephalopathy. At the same time, a single, even severe, insulin coma is accompanied by reversible metabolic changes in the brain. Therefore, the pathological features of metabolism in the nervous tissue, which are the result of repeated hypoglycemia, in particular possible disturbances in energy metabolism, require further study. In this work, we studied the main ways of glucose metabolism - the intensity of glycolysis and glycogenolysis, the activity of Krebs cycle dehydrogenases, alanine and aspartate aminotransferases in the rat brain in setting of multiple hypoglycemia.

Author(s):  
Pratik Choudhary ◽  
Stephanie A. Amiel

Hypoglycaemia (low blood glucose concentration) is the most important acute complication of the pharmacological treatment of diabetes mellitus. Low blood glucose impairs brain (and, potentially, cardiac) function. The brain has minimal endogenous stores of energy, with small amounts of glycogen in astroglial cells. The brain is therefore largely dependent on circulating glucose as the substrate to fuel cerebral metabolism and support cognitive performance. If blood glucose levels fall sufficiently, cognitive dysfunction is inevitable. In health, efficient glucose sensing and counterregulatory mechanisms exist to prevent clinically significant hypoglycaemia. These are impaired by diabetes and by its therapies. Patients with diabetes rank fear of hypoglycaemia as highly as fear of chronic complications such as nephropathy or retinopathy (1). Fear of hypoglycaemia, hypoglycaemia itself and attempts to avoid hypoglycaemia limit the degree to which glycaemic control can be intensified to reduce the risk of chronic complications of diabetes both for type 1 and type 2 diabetes.


2020 ◽  
Vol 56 (3) ◽  
pp. 224-234
Author(s):  
A. A. Soldatov ◽  
I. V. Golovina ◽  
E. E. Kolesnikova ◽  
I. V. Sysoeva ◽  
A. A. Sysoev ◽  
...  

2014 ◽  
Vol 36 (3) ◽  
pp. 220-226 ◽  
Author(s):  
Gabriela K. Ferreira ◽  
Mariane R. Cardoso ◽  
Isabela C. Jeremias ◽  
Cinara L. Gonçalves ◽  
Karolina V. Freitas ◽  
...  

2022 ◽  
Vol 15 ◽  
Author(s):  
Hao Lei ◽  
Rong Hu ◽  
Guanghua Luo ◽  
Tingqian Yang ◽  
Hui Shen ◽  
...  

Type 2 diabetes mellitus (T2DM) is associated with cognitive impairment in many domains. There are several pieces of evidence that changes in neuronal neuropathies and metabolism have been observed in T2DM. Structural and functional MRI shows that abnormal connections and synchronization occur in T2DM brain circuits and related networks. Neuroplasticity and energy metabolism appear to be principal effector systems, which may be related to amyloid beta (Aβ) deposition, although there is no unified explanation that includes the complex etiology of T2DM with cognitive impairment. Herein, we assume that cognitive impairment in diabetes may lead to abnormalities in neuroplasticity and energy metabolism in the brain, and those reflected to MRI structural connectivity and functional connectivity, respectively.


Author(s):  
Janusz Błaszczyk

A growing body of evidence indicates that aging of the brain is strictly related to the decline of energy metabolism. In particular, in older adults, the neuronal metabolism of glucose declines steadily resulting in a growing deficit of ATP production. The decline is evoked by deficient NAD recovery in the salvage pathway and subsequent impairment of the Krebs cycle. NAD deficit impairs also the activity of NAD-dependent enzymes. All these open vicious circles of neurodegeneration and neuronal death. Some brain structures are particularly prone to aging and neurodegeneration. These are pathological foci of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. This review article summarizes the impacts and mutual relationships between metabolic processes both on neuronal and brain levels. It also provides directions on how to reduce the risk of neurodegeneration and protect the elderly against neurodegenerative diseases.


Author(s):  
A. M. Rashidova

Aim. The aim of this work was to give a review of own studies of dynamics of the activity of energy metabolism enzymes in the brain during postnatal ontogenesis which characterizes the functional relations within the analysers, the destruction of their functions and the impact of adverse environmental factors on the body as well. Methods. The methods for the determination of the activity of energy metabolism enzymes in the brain of animals under the impact of adverse environmental factors and dysfunction of the analysers have been used. Results. It has been stated that the enzyme activity is regionally different in the tissues and sub cellular fractions of the brain depending on the animal species and the degree of the intensity of the stress factors, age and sex of the animal, circadian rhythms, season andmoreover, the resulting changes in the enzyme activity in most casesare irreversible. Conclusions. The data allow the dynamics of the activity of the energy supply enzymes to be considered as a determinant of cell reaction in response to exposure to adverse environmental factors and disturbance of sensory impulsation, which results in temporary increasing in the protection of intracellular energy metabolism through the development of an adaptive brain response.Key words: ontogenesis, brain, analysers, enzymes, environmental factors.


2013 ◽  
Vol 17 (2 (66)) ◽  
pp. 140-142
Author(s):  
O. A. Khodakivskyi

In experiments on rats with a model acute disorder of the cerebral circulation (bilateral carotid occlusion) it has been established that the introduction of a derivative adamantane 1-adamantiletiloxy-3-morpholino-2 propanol hydrochloride (under a conventional name ademol) in a dose of 2 mg/kg intraabdominally in the treatment mode (in an hour after insult and further 1 time per diem in every 24 hours during 4 days of cerebral ischemia) better than the cerebral protector cytikolin contributes to a decrease of disorders of carbohydrate and energy metabolism. A similar effect of ademol is one of the key mechanisms of its protective influence on ischemized neurons of the brain, pointing out to its perspective for the creation on its basis of a new cerebroprotective agent.


1999 ◽  
Vol 138 (4) ◽  
pp. s334-s337 ◽  
Author(s):  
S RAO ◽  
A BETHEL ◽  
M FEINGLOS

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2293-PUB ◽  
Author(s):  
VEERANNA KARADI ◽  
DILIP PAWAR ◽  
SARAH JABEEN ◽  
SANDEEP S. ◽  
SAPTARSHI BOSE ◽  
...  

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