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Query: UMLS:C0011860 (
type 2 diabetes
)
57,723
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Age-related macular degeneration
(
ARMD
) is one of the leading causes of vision impairment in the elderly and its frequency in general population increases with aging. The etiology of this disease has remained so far unknown. The relationship between
ARMD
and diabetes mellitus was studied in the present work. Fundus oculi was investigated in 292 diabetic patients older than 50 years and with more than 14 years of duration of diabetes (time since diagnosis). A group of 375 non diabetic, non hypertensive subjects matched for age was studied as control.
ARMD
frequency was significantly higher in diabetics compared to controls (p < 0.005); and also in type II diabetics (
non-insulin dependent diabetes mellitus
=
NIDDM
) compared to type I (insulin dependent diabetes mellitus = IDDM) (p < 0.001). Older diabetic patients showed an increased frequency of
ARMD
while no correlation with the duration of the disease emerged. Macular damage was not linked to microangiopathy (retinopathy), hypertension or gender; on the contrary, it appeared to be associated with dyslipidemia. On the basis of these data one can conclude that diabetes mellitus can exert an unfavorable effect on macular age-related phenomena even if the pathogenetic mechanism is at present obscure.
...
PMID:Age-related macular disease in diabetes mellitus. 1865 80
The panoply of treatment algorithms, periodically released to improve guidance, is one mean to face therapeutic uncertainty in pharmacological management of hyperglycemia in
type 2 diabetes
, especially after metformin failure. Failure of recent guidelines to give advice on the use of specific antidiabetic drugs in patients with co-morbidity may generate further uncertainty, given the frequent association of
type 2 diabetes
with common comorbidity, including, although not limited to obesity, cardiovascular disease, impaired renal function, and frailty. The Italian Association of Diabetologists (Associazione Medici Diabetologi,
AMD
) recognized the need to develop personalized treatment plans for people with
type 2 diabetes
, taking into account the patients' individual profile (phenotype), with the objective of the safest possible glycemic control. As not every subject with
type 2 diabetes
benefits from intensive glycemic control, flexible regimens of treatment with diabetes drugs (including insulin) are needed for reaching individualized glycemic goals. Whether personalized diabetology will improve the quality healthcare practice of diabetes management is unknown, but specific research has been launched.
...
PMID:Management of hyperglycemia in type 2 diabetes: evidence and uncertainty. 2372 Nov 70
Diabetic macular edema (DME) and diabetic retinopathy (DR) are complications affecting about 25% of all patients with long-standing type 1 and
type 2 diabetes
mellitus and are a major cause of significant decrease in vision and quality of life.
Age-related macular degeneration
(
AMD
) is not uncommon, and diabetes mellitus affects the incidence and progression of
AMD
through altering hemodynamics, increasing oxidative stress, accumulating advanced glycation end products, etc. Recent studies suggest that DME, DR and
AMD
are inflammatory conditions characterized by a breakdown of the blood-retinal barrier, inflammatory processes and an increase in vascular permeability. Key factors that seem to have a dominant role in DME, DR and
AMD
are angiotensin II, prostaglandins and the vascular endothelial growth factor and a deficiency of anti-inflammatory bioactive lipids. The imbalance between pro- and anti-inflammatory eicosanoids and enhanced production of pro-angiogenic factors may initiate the onset and progression of DME, DR and
AMD
. This implies that bioactive lipids that possess anti-inflammatory actions and suppress the production of angiogenic factors could be employed in the prevention and management of DME, DR and
AMD
.
...
PMID:Diabetic macular edema, retinopathy and age-related macular degeneration as inflammatory conditions. 2769 6
Age-related macular degeneration
(
AMD
) is a leading cause of blindness with limited effective treatment. Although the pathogenesis of this disease is complex and not fully understood, the oxidative damage caused by excessive reactive oxygen species (ROS) in retinal pigment epithelium (RPE) has been considered as a major cause. Autophagy is essential for the degradation of cellular components damaged by ROS, and its dysregulation has been implicated in
AMD
pathogenesis. Therefore, strategies aiming to boost autophagy could be effective in protecting RPE cells from oxidative damage. Metformin is the first-line anti-
type 2 diabetes
drug and has been reported to stimulate autophagy in many tissues. We therefore hypothesized that metformin may be able to protect RPE cells against H
2
O
2
-induced oxidative damage by autophagy activation. In the present study, we found that metformin attenuated H
2
O
2
-induced cell viability loss, apoptosis, elevated ROS levels, and the collapse of the mitochondria membrane potential in D407 cells. Autophagy was stimulated by metformin, and inhibition of autophagy by 3-methyladenine (3-MA) and chloroquine (CQ) or knockdown of Beclin1 and LC3B blocked the protective effects of metformin. In addition, we showed that metformin could activate the AMPK pathway, whereas both pharmacological and genetic inhibitions of AMPK blocked the autophagy-stimulating and protective effects of metformin. Metformin conferred a similar protection against H
2
O
2
-induced oxidative damage in primary cultured human RPE cells. Taken together, these results demonstrate that metformin could protect RPE cells from H
2
O
2
-induced oxidative damage by stimulating autophagy via the activation of the AMPK pathway, supporting its potential use in the prevention and treatment of
AMD
.
...
PMID:Protective Effect of Metformin against Hydrogen Peroxide-Induced Oxidative Damage in Human Retinal Pigment Epithelial (RPE) Cells by Enhancing Autophagy through Activation of AMPK Pathway. 3277 66
