Cinnamic Acid and Its Derivatives: Mechanisms for Prevention and Management of Diabetes and Its Complications.

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Term Occurence Count Dictionary
obesity 2 endocrinologydiseases
type 2 diabetes mellitus 3 endocrinologydiseases
Insulin 5 endocrinologydiseasesdrugs
amyloidosis 3 endocrinologydiseases
diabetes mellitus 3 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
hypoglycemia 2 endocrinologydiseases
acarbose 5 endocrinologydiseasesdrugs
hyperglycemia 11 endocrinologydiseases
metformin 9 endocrinologydiseasesdrugs
sitagliptin 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 9676 beneficial effects of cinnamic acid and its derivatives related to diabetes and its complications.3.1. Insulin SecretionElevated circulating concentration of glucose is mainly regulated by insulin secretion from
Insulin 61356 cinnamic acid and its derivatives on inhibition of protein glycation are demonstrated in Table 6.3.12. Insulin FibrillationInsulin fibrillation, characterized by β-sheet rich structure, is present in arterial walls
Insulin 61376 derivatives on inhibition of protein glycation are demonstrated in Table 6.3.12. Insulin Fibrillation Insulin fibrillation, characterized by β-sheet rich structure, is present in arterial walls and on membrane
Insulin 67635 derivatives could stimulate insulin secretion and improve pancreatic β-cell functionality.MechanismsEffects Insulin secretionm-Hydroxycinnamic acid, p-methoxycinnamic acid, and ferulic acid stimulate insulin secretion
Insulin 75918 serumCaffeic acid inhibits methylglyoxal-induced protein glycation in bovine serum albumin and histone Insulin fibrillationFerulic acid inhibits the formation of insulin amyloid fibri
acarbose 44816 (IC50 value = 0.49 mM) was a non-competitive inhibition [[88]]. The combined concentration between acarbose and cinnamic acids derivatives on the inhibition of α-glucosidase has been noted in this study [[88]].
acarbose 45094 acid could produce additive intestinal sucrase inhibition when combination with low concentration of acarbose . Boath et al. suggest that phytochemical compounds with high α-glucosidase and lower pancreatic α-amylase
acarbose 45269 α-glucosidase and lower pancreatic α-amylase inhibitory activity could prevent certain side effects of acarbose [[89]]. The decreasing required dose of acarbose by combined with phytochemical compounds might diminish
acarbose 45318 inhibitory activity could prevent certain side effects of acarbose [[89]]. The decreasing required dose of acarbose by combined with phytochemical compounds might diminish its gastrointestinal side effects such as flatulence,
acarbose 46910 acid derivatives led to an increased potency against intestinal maltase with equivalent potency as acarbose [[94]].Narita et al. described the inhibitory effects of cinnamic acid derivatives on porcine α-amylase
metformin 18489 STZ-induced diabetic rats [[44]]. Ferulic acid (10 and 40 mg/kg) exhibited synergistic effect with metformin and thiazolidinedione on the improvement of blood glucose and lipid profile in STZ-induced diabetic
metformin 18804 reduced insulitis grades near to normal values were observed when co-administration of ferulic acid and metformin or thiazolidinedione. The increased β-cell mass improved the ability to secrete insulin which might
metformin 23920 acid, p-hydroxycinnamic acid, and caffeic acid) and their combinations with oral hypoglycemic drugs ( metformin and thiazolidinedione) has been described to promote synergistic effect in the glucose uptake activity
metformin 24598 hypoglycemic agents, ferulic acid, caffeic acid, and p-hydroxycinnamic acid synergistically interacted with metformin (20 μM) and thiazolidinedione (20 μM), whereas cinnamic acid exhibited an additive effect on the uptake
metformin 24824 glucose. The synergistic effect was also observed in rat L6 myotubes when combination of ferulic acid with metformin or thiazolidinedione [[44]]. The increase in mRNA expression of PI3K was detected when L6 myotubes were
metformin 31967 concentration, activity of glycogen synthase, and glucokinase restored to normal level similar to that of metformin after treatment of ferulic acid. The mRNA expression of PEPCK and glucose-6-phosphatase and the interaction
metformin 68652 increases islet number and sizes and reduced insulitis grades in diabetic rats when co-administration with metformin and thiazolidinedioneCinnamic acid prevents palmitic acid-induced lipotoxicity in mouse NIT-1 pancreatic
metformin 69791 3T3-L1 adipocytesFerulic acid, caffeic acid, and p-hydroxycinnamic acid synergistically interacted with metformin and thiazolidinedione, whereas cinnamic acid exhibited an additive effect on the uptake of glucoseCombination
metformin 69932 cinnamic acid exhibited an additive effect on the uptake of glucoseCombination of ferulic acid with metformin or thiazolidinedione demonstrates synergistic effect on glucose uptake in rat L6 myotubesFerulic acid
sitagliptin 20741 is a new therapeutic approach for management of type 2 diabetes [[48]]. DPP-IV inhibitors, such as sitagliptin and saxagliptin, slow the inactivation and degradation of glucagon-like peptide-1 (GLP-1) that stimulates
Select Disease Character Offset Disease Term Instance
amyloidosis 53072 Alzheimer’s disease [[109]]. The accumulation of amyloid cross β-structures induces pancreatic islet amyloidosis that results in β-cell damage and impaired insulin secretion in diabetic patients [[110]]. Ferulic
amyloidosis 53469 amyloid cross β-structures by these compounds may help reduce the progression of pancreatic islet amyloidosis .Molecular docking studies further characterized the interaction between cinnamic acid and its derivatives
amyloidosis 62721 interactions [[131]]. It is proposed that ferulic acid can be considered for delaying the growth of amyloidosis .4. New Formulation of Cinnamic Acid and Its DerivativesData on the bioavailability and other pharmacokinetic
diabetes mellitus 2050 to insulin resistance, impaired insulin signaling, and β-cell dysfunction. The prevalence of type 2 diabetes mellitus has increased dramatically in epidemic proportions worldwide that is one of the most important health
diabetes mellitus 2561 mortality and morbidity [[2]]. Nowadays, the general guidelines for treatment and management of type 2 diabetes mellitus recommend dietary modification including other aspects of lifestyle modification by increased the quantity
diabetes mellitus 3765 SGLT2 inhibitors are currently integrated as second- or third-line therapy for the treatment of type 2 diabetes mellitus [[6]]. However, oral hypoglycemic agents could produce severe hypoglycemia, weight gain, and gastrointestinal
hyperglycemia 1894 diabetic patients.1. IntroductionType 2 diabetes is a group of metabolic disorder characterized by hyperglycemia dyslipidemia, and protein metabolism due to insulin resistance, impaired insulin signaling, and β-cell
hyperglycemia 2214 proportions worldwide that is one of the most important health and socioeconomic problems [[1]]. Long-term hyperglycemia causes the development and progression of pathogenic conditions including micro- and macro-vascular
hyperglycemia 15146 insulin secretion are summarized in Table 1.3.2. Pancreatic β-Cell FunctionalityChronic exposure to hyperglycemia can lead to glucotoxicity that pertains to the dysfunction of pancreatic β-cell characterized by decreasing
hyperglycemia 22039 adipose tissue and skeletal muscle are main targets of insulin-stimulated glucose uptake to control of hyperglycemia . In skeletal muscle and adipose tissues, insulin-stimulated glucose uptake primarily occurs through
hyperglycemia 31228 p-methoxycinnamic acid. It was speculated that p-methoxycinnamic acid might play a major role in the control of hyperglycemia by decreasing hepatic glucose production in the insulin deficiency state.Ferulic acid (0.05 g/kg/day)
hyperglycemia 33843 supplementation of 0.05% ferulic acid alleviated high-fat and high-fructose diet-induced obesity, hyperlipidemia, hyperglycemia , hepatic injury, and insulin resistance in rats [[70]]. In vitro models confirmed that ferulic acid
hyperglycemia 34416 induced diabetic rats [[71]]. The orally administered p-hydroxycinnamic acid (100 mg/kg) attenuated hyperglycemia and hepatic glucose output via downregulation the expression of liver gluconeogenic enzymes (glucose-6-phosphatase
hyperglycemia 42600 of starch and disaccharides to absorbable monosaccharides, which suppresses a rise on postprandial hyperglycemia . This has been proved to be one of the effective strategies to decrease the postprandial rise in blood
hyperglycemia 48036 monosaccharides glucose from the intestinal tract could have substantial impact in controlling postprandial hyperglycemia [[96]]. Dietary glucose derived either from hydrolysis of starch or from sucrose is mainly taken up
hyperglycemia 49700 derivatives on inhibition of glucose absorption are summarized in Table 5.3.11. Protein GlycationLong-term hyperglycemia is a major causative factor to induce non-enzymatic protein glycation by reducing sugars, such as glucose
hyperglycemia 57114 intracellular glucose [[116]]. There was evidence indicating that ferulic acid (0.1–100 μM) improved hyperglycemia -induced impairment of Na+/K+-ATPase activity and reduced the formation of lipid peroxidation in glycated
hyperlipidemia 33827 that supplementation of 0.05% ferulic acid alleviated high-fat and high-fructose diet-induced obesity, hyperlipidemia , hyperglycemia, hepatic injury, and insulin resistance in rats [[70]]. In vitro models confirmed that
hypoglycemia 3845 treatment of type 2 diabetes mellitus [[6]]. However, oral hypoglycemic agents could produce severe hypoglycemia , weight gain, and gastrointestinal disturbances. In the last decade, dietary polyphenols have received
hypoglycemia 13822 normal rats. The overall findings suggest that p-methoxycinnamic acid improves glucose tolerance without hypoglycemia , which may be beneficial to diabetic conditions that have defects in the response of insulin secretion
obesity 33818 reported that supplementation of 0.05% ferulic acid alleviated high-fat and high-fructose diet-induced obesity , hyperlipidemia, hyperglycemia, hepatic injury, and insulin resistance in rats [[70]]. In vitro models
obesity 37199 differentiation, which plays critical role on adipose tissue deposition and dysfunction, leading to induce obesity and insulin resistance. The suppressing adipogenesis-related gene expressions such as PPARγ and C/EBPα
type 2 diabetes mellitus 2043 metabolism due to insulin resistance, impaired insulin signaling, and β-cell dysfunction. The prevalence of type 2 diabetes mellitus has increased dramatically in epidemic proportions worldwide that is one of the most important health
type 2 diabetes mellitus 2554 of mortality and morbidity [[2]]. Nowadays, the general guidelines for treatment and management of type 2 diabetes mellitus recommend dietary modification including other aspects of lifestyle modification by increased the quantity
type 2 diabetes mellitus 3758 (EASD), SGLT2 inhibitors are currently integrated as second- or third-line therapy for the treatment of type 2 diabetes mellitus [[6]]. However, oral hypoglycemic agents could produce severe hypoglycemia, weight gain, and gastrointestinal

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