Huntington's Disease and Diabetes: Chronological Sequence of its Association.

Existing Reviews

Please note, new claims can take a short while to show up.

No claims yet.

Annotation Summary

Term Occurence Count Dictionary
Insulin 3 endocrinologydiseasesdrugs
cortisol 2 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
metformin 6 endocrinologydiseasesdrugs
rosiglitazone 4 endocrinologydiseasesdrugs
testosterone 1 endocrinologydiseasesdrugs
Exenatide 5 endocrinologydiseasesdrugs
diabetic ketoacidosis 1 endocrinologydiseases
hyperglycemia 3 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

Note: If this graph is empty, then there are no terms that meet the proximity constraint.

Review

Having read the paper, please pick a pair of statements from the paper to indicate that a drug and disease are related.

Select Drug Character Offset Drug Term Instance
Exenatide 18260 modificationR6/2MetforminNo modificationNo modification–––Partial improvementIncreased 20.1% in malesR6/2 Exenatide IncreasedReducedReducedIncreasedSignificant improvementSignificant improvementIncreased 18% in malesN171-82QGLP-1-TfNo
Exenatide 19167 insulin sensitization among other positive effects on glucose transport and hepatic glucose synthesis–; Exenatide – antidiabetic glucagon-like peptide (GLP-1) receptor agonist (58)–; GLP-1Tf – a fusion protein
Exenatide 19996 modified the extreme and uncontrolled weight loss observed in the HD model during the disease progression. Exenatide treatment exacerbated the reduction, as previously described in human subjects and animal models [[56]].
Exenatide 20466 alone suggests that insulin resistance is not a primary factor in diabetes occurring in HD mice [[21]]. Exenatide and GLP-1Tf were able to reduce glucose levels; however, the insulin treatment had no effect on the
Exenatide 21920 islets; while no positive modification in pancreatic morphology was induced by insulin treatment [[56]]. Exenatide – approved for the treatment of type-2 diabetes (T2D)–was the most beneficial therapy for diabetic
Insulin 17922 1Treatments with hypoglycemic agents in HD murine modelsWeight lossPlasma glucose levelPlasma insulin level Insulin sensitivityPancreatic morphologyMotor coordinationLife spanMurine modelGlibenclamideNo modificationReduced–––No
Insulin 18491 modificationReducedIncreased–Significant improvementPartial improvementIncreased 17% in malesN171-82Q Insulin No modificationNo modificationIncreased–No modificationReducedNo modificationN171-82QResveratrolNo
Insulin 19346 (58)–; GLP-1Tf – a fusion protein made up of GLP-1 and nonglycosylated form of human transferrin–; Insulin – the basic treatment for type 1 diabetes, and frequently used in long standing T2D to achieve adequate
cortisol 3865 conducted by the hypothalamic-endocrine axis [[11]]. HD subjects show endocrine changes such as increased cortisol levels and reduced testosterone values [[12]]. Beyond that, some researches have described abnormalities
cortisol 7663 fasting blood glucose level and glucose response to insulin were similar. However, the response of plasma cortisol and of GH to hypoglycemia was earlier in the HD patients, though peak responses were the same. These
metformin 18995 – increases insulin sensitivity by activating the peroxisome proliferator-activated receptor γ–; metformin – a widely antidiabetic drug, and also, an inducer of insulin sensitization among other positive effects
metformin 19763 treatments administered to R6/2 or N171-82Q mice were glibenclamide in combination with rosiglitazone, metformin , exenatide, insulin, GLP-1Tf, and resveratrol [[53]]. With the exception of exenatide, none of the compounds
metformin 20291 after the administration of glibenclamide/rosiglitazone, exenatide, GLP-1-Tf, and resveratrol, but not metformin [[59]]. The lack of glucose-level reduction by rosiglitazone alone suggests that insulin resistance
metformin 21036 nor resveratrol treatment influenced motor coordination in the animals. However, a 2-mg/ml dose of metformin decreased hind limb clasping time, while exenatide produced a reversal of motor performance decline,
metformin 21529 degree of progressive decline in motor performance, exerting no influence on life span. Nonetheless, metformin , exeantide, and GLP-1t induced a significant increase of survival (20%, 18 and 17, respectively). Both
metformin 27089 reported in China in 2009. No data were available concerning the influence of antidiabetic treatment ( metformin alone or in combination with insulin) in promoting or delaying the symptoms of HD [[73]].A curious case
rosiglitazone 19748 actions.The treatments administered to R6/2 or N171-82Q mice were glibenclamide in combination with rosiglitazone , metformin, exenatide, insulin, GLP-1Tf, and resveratrol [[53]]. With the exception of exenatide, none
rosiglitazone 20230 blood glucose levels, a significant decrease was observed after the administration of glibenclamide/ rosiglitazone , exenatide, GLP-1-Tf, and resveratrol, but not metformin [[59]]. The lack of glucose-level reduction
rosiglitazone 20348 exenatide, GLP-1-Tf, and resveratrol, but not metformin [[59]]. The lack of glucose-level reduction by rosiglitazone alone suggests that insulin resistance is not a primary factor in diabetes occurring in HD mice [[21]].
rosiglitazone 20923 though no information related to sensitivity to the hormone was available [[60]]. Neither glibenclamide, rosiglitazone nor resveratrol treatment influenced motor coordination in the animals. However, a 2-mg/ml dose of metformin
testosterone 3893 hypothalamic-endocrine axis [[11]]. HD subjects show endocrine changes such as increased cortisol levels and reduced testosterone values [[12]]. Beyond that, some researches have described abnormalities of carbohydrate metabolism
Select Disease Character Offset Disease Term Instance
diabetes mellitus 8199 above, the participants had not been diagnosed with diabetes. Interestingly, a higher prevalence of diabetes mellitus in patients with HD – specifically among the probands under 50 years of age–was reported by a retrospective
diabetes mellitus 12115 R6/2 mice, which exhibited no increase in blood glucose levels in diurnal profiles, suggesting latent diabetes mellitus [[18]]. Although at 12 weeks a decrease in glucose utilization is reported while a large elevation of
diabetic ketoacidosis 27679 hyperglycemia-induced-chorea-ballism is predominantly observed in T2D and very rare in type 1 diabetes (T1D) and diabetic ketoacidosis (DKA) a unique case of HD un-masked by an episode of chorea-ballism associated with DKA and T1D also
hyperglycemia 11791 gait, and stereotypic and abrupt movements (9 weeks of age), polyuria was present and the severity of hyperglycemia increased in the already high-glucose-level mice, while the remaining mice were euglycemic. Moreover,
hyperglycemia 12821 R6/2 model was the main contributing factor to onset of diabetes [[21]]. Stress is known to enhance hyperglycemia in altered metabolic states [[44]], and it induced the activation of the protein kinase (SAPK) pathway,
hyperglycemia 27566 though diabetes was not a major contributor to the HD phenotype [[74]]. On the other hand, although hyperglycemia -induced-chorea-ballism is predominantly observed in T2D and very rare in type 1 diabetes (T1D) and diabetic
hypoglycemia 7685 and glucose response to insulin were similar. However, the response of plasma cortisol and of GH to hypoglycemia was earlier in the HD patients, though peak responses were the same. These findings could be due to

You must be authorized to submit a review.