Last update 01 Nov 2024

Pantothenic acid deficiency

Last update 01 Nov 2024

Basic Info

Synonyms

Deficiency of pantothenic acid, Pantothenic acid deficiency, Pantothenic acid deficiency (disorder)

+ [6]

Introduction-

Drugs associated with Pantothenic acid deficiency

Pantethine

Target

Mechanism

RT inhibitors

Active Org.

Alfresa Pharma Corp.

Originator Org.

Alfresa Pharma Corp.

Active Indication

Pantothenic acid deficiency

Inactive Indication

Cataract

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date28 Sep 1977

Dexpanthenol

Target

mAChRs

Mechanism

mAChRs agonists

Active Org.

TOA Eiyo Ltd.

Originator Org.

TOA Eiyo Ltd.

Active Indication

Pantothenic acid deficiency [+1]

Inactive Indication

Diabetic Foot [+6]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date20 Mar 1959

100 Clinical Results associated with Pantothenic acid deficiency

100 Translational Medicine associated with Pantothenic acid deficiency

0 Patents (Medical) associated with Pantothenic acid deficiency

207

Literatures (Medical) associated with Pantothenic acid deficiency

01 Dec 2022·Animal Nutrition

Integrated liver proteomics and metabolomics identify metabolic pathways affected by pantothenic acid deficiency in Pekin ducks

Article

Author: Zhou, Zhengkui ; Zhang, Bo ; Xie, Ming ; Guo, Zhanbao ; Hu, Jian ; Tang, Jing ; Hou, Shuisheng ; Wu, Yongbao ; Liang, Suyun

Pantothenic acid deficiency (PAD) in animals causes growth depression, fasting hypoglycemia and impaired lipid and glucose metabolism. However, a systematic multi-omics analysis of effects of PAD on hepatic function has apparently not been reported. We investigated liver proteome and metabolome changes induced by PAD to explain its effects on growth and liver metabolic disorders. Pekin ducks (1-d-old, n = 128) were allocated into 2 groups, with 8 replicates and 8 birds per replicate. For 16 d, all ducks had ad libitum access to either a PAD or a pantothenic acid adequate (control, CON) diet, formulated by supplementing a basal diet with 0 or 8 mg pantothenic acid/kg of diet, respectively. Liver enlargement, elevated liver glycogen concentrations and decreased liver concentrations of triglyceride and unsaturated fatty acids were present in the PAD group compared to the CON group. Based on integrated liver proteomics and metabolomics, PAD mainly affected glycogen synthesis and degradation, glycolysis and gluconeogenesis, tricarboxylic acid (TCA) cycle, peroxisome proliferator-activated receptor (PPAR) signaling pathway, fatty acid beta oxidation, and oxidative phosphorylation. Selected proteins were confirmed by Western blotting. Downregulation of proteins and metabolites involved in glycogen synthesis and degradation, glycolysis and gluconeogenesis implied that these processes were impaired in PAD ducks, which could have contributed to fasting hypoglycemia, liver glycogen storage, insufficient ATP production, and growth retardation. In contrast, PAD also upregulated proteins and metabolites involved in fatty acid beta oxidation, the TCA cycle, and oxidative phosphorylation processes in the liver; presumably compensatory responses to produce ATP. We inferred that PAD decreased liver triglyceride and unsaturated fatty acids by activating fatty acid beta oxidation and impairing unsaturated fatty acid synthesis. These findings contributed to our understanding of the mechanisms of PAD-induced changes in hepatic metabolism.

01 Dec 2021·BMC GenomicsQ2 · BIOLOGY

Severe pantothenic acid deficiency induces alterations in the intestinal mucosal proteome of starter Pekin ducks

Q2 · BIOLOGY

ArticleOA

Author: Zhou, Zhengkui ; Wu, Yongbao ; Zhang, Bo ; Guo, Zhanbao ; Xie, Ming ; Tang, Jing ; Feng, Yulong ; Liang, Suyun ; Hou, Shuisheng

AbstractBackgroundPantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. However, the underlying molecular mechanisms remain to be elucidated. Mucosal proteome might reflect dietary influences on physiological processes.ResultsA total of 128 white Pekin ducks of one-day-old were randomly assigned to two groups, fed either a PAD or a pantothenic acid adequate (control, CON) diet. After a 16-day feeding period, two ducks from each replicate were sampled to measure plasma parameters, intestinal morphology, and mucosal proteome. Compared to the CON group, high mortality, growth retardation, fasting hypoglycemia, reduced plasma insulin, and oxidative stress were observed in the PAD group. Furthermore, PAD induced morphological alterations of the small intestine indicated by reduced villus height and villus surface area of duodenum, jejunum, and ileum. The duodenum mucosal proteome of ducks showed that 198 proteins were up-regulated and 223 proteins were down-regulated (> 1.5-fold change) in the PAD group compared to those in the CON group. Selected proteins were confirmed by Western blotting. Pathway analysis of these proteins exhibited the suppression of glycolysis and gluconeogenesis, fatty acid beta oxidation, tricarboxylic acid cycle, oxidative phosphorylation, oxidative stress, and intestinal absorption in the PAD group, indicating impaired energy generation and abnormal intestinal absorption. We also show that nine out of eleven proteins involved in regulation of actin cytoskeleton were up-regulated by PAD, probably indicates reduced intestinal integrity.ConclusionPAD leads to growth depression and intestinal hypofunction of ducks, which are associated with impaired energy generation, abnormal intestinal absorption, and regulation of actin cytoskeleton processes. These findings provide insights into the mechanisms of intestinal hypofunction induced by PAD.

01 Aug 2019·JGH Open

Causation of human ulcerative colitis: A lead from an animal model that mirrors human disease

Article

Author: Roediger, William E W

Most models of experimental colitis do not replicate human ulcerative colitis and do not help in defining the causation of human ulcerative colitis. Inducing pantothenic acid deficiency in pigs produces an ideal model in terms of extent, histology, and chronicity of human ulcerative colitis. Comparing metabolic changes in human ulcerative colitis with metabolic changes in experimental colitis in pigs provided a guide for the search of initiating factors of human ulcerative colitis. Observations showed that bacterial nitric oxide with bacterial hydrogen sulphide reproduced the metabolic changes of human ulcerative colitis. Decreasing colon‐produced nitric oxide and hydrogen sulphide by bacteria through diet and medication resulted in pronounced therapeutic improvement, both clinically and histologically, of human ulcerative colitis.

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Pantothenic acid deficiency

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