Study of glycation process of human carbonic anhydrase II as well as investigation concerning inhibitory influence of 3-beta-hydroxybutyrate on it

Gharib, Raziyeh; Khatibi, Ali; Khodarahmi, Reza; Haidari, Masoumeh; Husseinzadeh, Susan

doi:10.1016/j.ijbiomac.2020.01.192

Cited by 14 publications

(7 citation statements)

References 49 publications

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“…Growing evidence concerning bone fracture in patients with diabetes mellitus indicates the crucial roles of AGEs in aggravating bone fragility (40). However, ketogenic diet improves glycemic control in type 2 diabetes (41), and 3-bhydroxybutyrate (the main component of a ketone body) inhibits the glycation process, decreases glucose binding to the protein, and prevents the formation of AGEs (42). Therefore, AGEs might not be a common role in the bone deterioration induced by hyperglycemia and hyperketonemia, but further study is needed.…”

Section: Discussionmentioning

confidence: 99%

The Hyperglycemia and Hyperketonemia Impaired Bone Microstructures: A Pilot Study in Rats

Zhou

Xie

et al. 2020

Front. Endocrinol.

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Though diabetes mellitus (DM) is one of the known causes of osteoporosis, it is also realized that ketogenic diet (KD), an effective regimen for epilepsy, impairs bone microstructures. However, the similarities and differences of effects between these two factors are still unknown. The purpose of this study is to identify different effects between hyperglycemia and hyperketonemia, which are manifestations of DM and KD, on bone in rats. Thirty male Sprague-Dawley rats were randomly divided into three groups: the sham, DM, and KD groups. Hyperglycemia was achieved by intravenous injection of streptozotocin in DM group, while hyperketonemia was induced by application of ketogenic diet (carbohydrates-to-fat as 1:3) in KD group. The body weight, blood ketone body, and blood glucose were recorded, and the bone turnover markers, bone length, bone microstructures, bone biomechanics and histomorphology were measured after 12 weeks intervention. Compared with the control and KD groups, a significant body weight loss was found in the DM group, and the bone lengths of tibia and femur of the group were shortened. The blood glucose and blood ketone were noticeably increased in the DM and KD rats, respectively. Microstructures and properties of cancellous bone were significantly deteriorated in both the DM and KD groups compared with the sham group, as the bone volumes were decreased and the bone trabecula structures were disturbed. Meanwhile, the thickness and strength of cortical bone was reduced more in the DM group than those in the sham and KD groups. The HE staining showed that bone trabecula was significantly decreased in both the DM and KD groups, and more adipose tissue was observed in the KD rats. The activity of osteoblasts was decreased more in both the KD and DM groups than that in the sham group, while the activity of osteoclasts of the two groups was remarkably increased. The present study indicates that both hyperglycemia and hyperketonemia have adverse effects on bone. Therefore, it is worth paying more attention to the bone status of patients with hyperglycemia and hyperketonemia in clinic.

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Section: Discussionmentioning

confidence: 99%

The Hyperglycemia and Hyperketonemia Impaired Bone Microstructures: A Pilot Study in Rats

Zhou

Xie

et al. 2020

Front. Endocrinol.

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“…When glycated CA I was purified from erythrocytes of diabetic patients, it was demonstrated to present a specific enzymatic activity that was approximately 40% of that of the non-modified enzyme from normal individuals 109 . Other studies on CA II demonstrated that extensive protein glycation is accompanied with a significant conformational change and a reduced enzymatic activity 110 . Above-mentioned investigations suggested that changes in general CA activity in human erythrocytes due to protein glycation can be considered among the initial steps of altered metabolism in diabetes 111 .…”

Section: Non-enzymatic Glycationmentioning

confidence: 97%

Human carbonic anhydrases and post-translational modifications: a hidden world possibly affecting protein properties and functions

Fiore

Supuran

Scaloni

et al. 2020

Journal of Enzyme Inhibition and Medicinal Chemistry

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Human carbonic anhydrases (CAs) have become a well-recognized target for the design of inhibitors and activators with biomedical applications. Accordingly, an enormous amount of literature is available on their biochemical, functional and structural aspects. Nevertheless post-translational modifications (PTMs) occurring on these enzymes and their functional implications have been poorly investigated so far. To fill this gap, in this review we have analysed all PTMs occurring on human CAs, as deriving from the search in dedicated databases, showing a widespread occurrence of modification events in this enzyme family. By combining these data with sequence alignments, inspection of 3 D structures and available literature, we have summarised the possible functional implications of these PTMs. Although in some cases a clear correlation between a specific PTM and the CA function has been highlighted, many modification events still deserve further dedicated studies.

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“…Recent experimental and clinical studies have demonstrated that a KD can improve insulin sensitivity as well as glucose homeostasis [ 121 - 123 ]. Further studies have shown that βHB, the main KBs in the brain, restrains insulin glycation, AGE accumulation [ 124 , 125 ], and liposomal lipid peroxidation to ultimately prevent microglial apoptosis [ 126 ]. Thus, we can speculate that the anti-inflammatory effects of KD could hinder the development of neurodegenerative diseases through increasing insulin sensitivity.…”

Section: Possible Anti-inflammatory Mechanisms Of Kdmentioning

confidence: 99%

Effects of Ketogenic Diet on Neuroinflammation in Neurodegenerative Diseases

et al. 2022

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The ketogenic diet (KD) is a low-carbohydrate, high-fat and adequate-protein diet. As a diet mimicking fasting, it triggers the production of ketone bodies (KBs) and brings the body into a state of ketosis. Recent and accumulating studies on humans and animal models have shown that KD is beneficial to neurodegenerative diseases through modulating central and peripheral metabolism, mitochondrial function, inflammation, oxidative stress, autophagy, and the gut microbiome. Complicated interplay of metabolism, gut microbiome, and other mechanisms can regulate neuroinflammation in neurodegenerative diseases by activating multiple molecular and cellular pathways. In this review, we detail the physiological basis of the KD, its functions in regulating neuroinflammation, and its protective role in normal brain aging and neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). We aimed to elucidate the underlying neuroinflammatory mechanisms of KD therapies in neurodegenerative diseases and provide novel insights into their application for neurodegenerative disease prevention and treatment.

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Study of glycation process of human carbonic anhydrase II as well as investigation concerning inhibitory influence of 3-beta-hydroxybutyrate on it

Cited by 14 publications

References 49 publications

The Hyperglycemia and Hyperketonemia Impaired Bone Microstructures: A Pilot Study in Rats

The Hyperglycemia and Hyperketonemia Impaired Bone Microstructures: A Pilot Study in Rats

Human carbonic anhydrases and post-translational modifications: a hidden world possibly affecting protein properties and functions

Effects of Ketogenic Diet on Neuroinflammation in Neurodegenerative Diseases

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