Posts Tagged ‘PUFA’s and diabetes’

What is Diabetes

Monday, August 29th, 2011

Diabetes is a chronic disease that occurs either when the pancreas does not produce enough insulin or when the body cannot effectively use the insulin it produces. Insulin is a hormone that regulates blood sugar. Hyperglycaemia, or raised blood sugar, is a common effect of uncontrolled diabetes and over time leads to serious damage to many of the body’s systems, especially the nerves and blood vessels.
Type 1 diabetes (previously known as insulin-dependent, juvenile or childhood-onset) is characterized by deficient insulin production and requires daily administration of insulin. The cause of type 1 diabetes is not known and it is not preventable with current knowledge.

Symptoms include excessive excretion of urine (polyuria), thirst (polydipsia), constant hunger, weight loss, vision changes and fatigue. These symptoms may occur suddenly.
Type 2 diabetes (formerly called non-insulin-dependent or adult-onset) results from the body’s ineffective use of insulin. Type 2 diabetes comprises 90% of people with diabetes around the world, and is largely the result of excess body weight and physical inactivity.

Symptoms may be similar to those of Type 1 diabetes, but are often less marked. As a result, the disease may be diagnosed several years after onset, once complications have already arisen.

Until recently, this type of diabetes was seen only in adults but it is now also occurring in children.
Gestational diabetes is hyperglycaemia with onset or first recognition during pregnancy.

Symptoms of gestational diabetes are similar to Type 2 diabetes. Gestational diabetes is most often diagnosed through prenatal screening, rather than reported symptoms.

Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG)
Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG) are intermediate conditions in the transition between normality and diabetes. People with IGT or IFG are at high risk of progressing to type 2 diabetes, although this is not inevitable.

What are common consequences of diabetes?
Over time, diabetes can damage the heart, blood vessels, eyes, kidneys, and nerves.

Diabetes increases the risk of heart disease and stroke. 50% of people with diabetes die of cardiovascular disease (primarily heart disease and stroke).
Combined with reduced blood flow, neuropathy in the feet increases the chance of foot ulcers and eventual limb amputation.
Diabetic retinopathy is an important cause of blindness, and occurs as a result of long-term accumulated damage to the small blood vessels in the retina. After 15 years of diabetes, approximately 2% of people become blind, and about 10% develop severe visual impairment.
Diabetes is among the leading causes of kidney failure. 10-20% of people with diabetes die of kidney failure.
Diabetic neuropathy is damage to the nerves as a result of diabetes, and affects up to 50% of people with diabetes. Although many different problems can occur as a result of diabetic neuropathy, common symptoms are tingling, pain, numbness, or weakness in the feet and hands.

UK experts are predicting a steep rise in the rate of an eye condition that is already a leading cause of blindness globally . Omega 3 EPA and DHA an reduce risk

Wednesday, July 13th, 2011

UK experts are predicting a steep rise in the rate of an eye condition that is already a leading cause of blindness globally . Omega 3 EPA and DHA an reduce risk

Age-related macular degeneration (AMD) affects more than 600,000 Britons.But an ageing population means this figure could rise by a quarter to nearly 756,000 by 2020, according to recent research in the British Journal of Ophthalmology.Yet half of UK adults have never heard of AMD, a poll by the College of Optometrists suggests.The survey of over 4,000 also found many people were unaware that a poor diet and smoking increases the risk of AMD.AMD affects a tiny part of the retina at the back of the eye that controls central vision.

people in UK and globally need to be more aware of AMD and the impact that it can have This makes it difficult for the individual to see fine detail, such as recognising people’s faces, reading or watching television.There are two forms of AMD, wet and dry.There is currently no cure for either forms but early diagnosis and treatment of wet AMD – which develops rapidly – is crucial in order to prevent vision loss.Dry AMD, which is more common, develops gradually and is not treatable but there are services available to support people with this condition.Dr Susan Blakeney, optometric adviser to the College of Optometrists said: “Age-related macular degeneration is the biggest single cause of sight loss in the UK so it is concerning that so few people are aware of it and its symptoms.”By making people more aware of AMD and the impact that it can have, we hope to increase detection and people seeking access to support services.”While AMD is a condition associated with older age, there are steps you can take earlier in life to minimise your risk.Research suggests that a diet rich in leafy green vegetables, brightly coloured fruits and vegetables and oily fish may help prevent AMD.Smoking also doubles your chances of developing the condition so quitting can also reduce your risk.Dr Blakeney said: “I also recommend to patients that they regularly check the vision in each eye separately so that they can spot early changes.”It is easy to do and only takes a couple of seconds, yet it could save your sight. You can do it by looking at a bit of graph paper and checking if you see any distortion or blank spots.”

Omega 3 fish oil benefits may prevent Diabetic retinopathy

Thursday, March 31st, 2011

RESEARCH ARTICLE
ANTI-ANGIOGENESIS
5-Lipoxygenase Metabolite 4-HDHA Is a Mediator of the Antiangiogenic Effect of ω-3 Polyunsaturated Fatty Acids
Przemyslaw Sapieha1,2,*, Andreas Stahl1,3,*, Jing Chen1, Molly R. Seaward1, Keirnan L. Willett1, Nathan M. Krah1, Roberta J. Dennison1, Kip M. Connor1,†, Christopher M. Aderman1, Elvira Liclican4, Arianna Carughi5,6, Dalia Perelman5,6, Yoshihide Kanaoka7, John Paul SanGiovanni8, Karsten Gronert4 and Lois E. H. Smith1,‡
+ Author Affiliations

1Department of Ophthalmology, Harvard Medical School, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
2Department of Ophthalmology, Maisonneuve-Rosemont Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada H1T 2M4.
3University Eye Hospital Freiburg, Killianstrasse 5, Freiburg 79106, Germany.
4Vision Science Program, School of Optometry, University of California, Berkeley, CA 94720, USA.
5Health Research and Studies Center, Los Altos, CA 94022, USA.
6Palo Alto Medical Foundation, Palo Alto, CA 94301, USA.
7Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA 02115, USA.
8Division of Epidemiology and Clinical Research, National Eye Institute, Bethesda, MD 20892, USA
‡To whom correspondence should be addressed. E-mail: lois.smith@childrens.harvard.edu
ABSTRACT

Lipid signaling is dysregulated in many diseases with vascular pathology, including cancer, diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. We have previously demonstrated that diets enriched in ω-3 polyunsaturated fatty acids (PUFAs) effectively reduce pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy, in part through metabolic products that suppress microglial-derived tumor necrosis factor–α. To better understand the protective effects of ω-3 PUFAs, we examined the relative importance of major lipid metabolic pathways and their products in contributing to this effect. ω-3 PUFA diets were fed to four lines of mice deficient in each key lipid-processing enzyme (cyclooxygenase 1 or 2, or lipoxygenase 5 or 12/15), retinopathy was induced by oxygen exposure; only loss of 5-lipoxygenase (5-LOX) abrogated the protection against retinopathy of dietary ω-3 PUFAs. This protective effect was due to 5-LOX oxidation of the ω-3 PUFA lipid docosahexaenoic acid to 4-hydroxy-docosahexaenoic acid (4-HDHA). 4-HDHA directly inhibited endothelial cell proliferation and sprouting angiogenesis via peroxisome proliferator–activated receptor γ (PPARγ), independent of 4-HDHA’s anti-inflammatory effects. Our study suggests that ω-3 PUFAs may be profitably used as an alternative or supplement to current anti–vascular endothelial growth factor (VEGF) treatment for proliferative retinopathy and points to the therapeutic potential of ω-3 PUFAs and metabolites in other diseases of vasoproliferation. It also suggests that cyclooxygenase inhibitors such as aspirin and ibuprofen (but not lipoxygenase inhibitors such as zileuton) might be used without losing the beneficial effect of dietary ω-3 PUFA.

↵* These authors contributed equally to this work.
↵† Present address: Massachusetts Eye and Ear Infirmary, Angiogenesis Laboratory, Department of Ophthalmology, Harvard Medical School, 243 Charles Street, Boston, MA 02114, USA.
Citation: P. Sapieha, A. Stahl, J. Chen, M. R. Seaward, K. L. Willett, N. M. Krah, R. J. Dennison, K. M. Connor, C. M. Aderman, E. Liclican, A. Carughi, D. Perelman, Y. Kanaoka, J. P. SanGiovanni, K. Gronert, L. E. H. Smith, 5-Lipoxygenase Metabolite 4-HDHA Is a Mediator of the Antiangiogenic Effect of ω-3 Polyunsaturated Fatty Acids. Sci. Transl. Med. 3, 69ra12 (2011).

Omega 3 fish oil may help activate anti-diabetic genes

Tuesday, March 8th, 2011

Fish oils may help to activate anti-diabetic genes

Polyunsaturated fatty acid fish oils may activate genes that regulate fat cell differentiation and glucose homeostasis, according to new research on mice.

The new study published in Journal of Nutritional Biochemistry suggests supplementation with omega3 fish oil activates the transcription factor PPARγ, increasing regulation of adipocytes and helps to maintain glucose homeostasis.

“We demonstrated that adipogenic genes and glucose metabolism genes were elevated in PPARγ transgenic mice when fed fish oil. This transgenic mouse model provided direct evidence to demonstrate omega 3 , especially EPA  regulate glucose homeostasis through interaction with PPARγ,” wrote the researchers, led by Dr Yu-Hsiang Yu from the National Taiwan University

Vital roles

Peroxisome-proliferator-activated receptor γ (PPARγ) is considered an important transcription factor in regulating fat cell (adipocyte) differentiation, and is also known to play a vital role in maintaining glucose homeostasis. The transcription factor is a target for many anti-diabetic drugs as activation promotes glucose dispersal.

Activation of PPARγ occurs through the binding of specific ligand molecules; however, polyunsaturated fatty acids such as arachidonic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are also known to have a high binding affinity for PPARγ.

Previous studies suggest that polyunsaturated fatty acids (PUFA) and their metabolites are able to regulate PPARγ activity, demonstrating that DHA treatment increases PPARγ-responsive gene expression in a cell model.

However, most research demonstrating PPARγ activity uses in vitro cell models and there is currently no direct evidence available to demonstrate that polyunsaturated fatty acids are able to activate PPARγ in vivo.

The authors said the current experiment was designed to determine the potential for PUFA, particularly EPA and DHA, to activate the function of PPARγ in vivo.

Wild-type and transgenic mice – with over expressed PPARγ –were supplemented with either fish oil or PPARγ ligands (rosiglitazone) for four months to investigate whether fish oils have similar effects to true PPARγ ligands in vivo.

Results

Dietary rosiglitazone fed mice had a significantly lower feed intake, but had no significant effect on body weight or fat pad weigh, whereas fish oil supplementation did not significantly decrease feed intake, but significantly decreased body and fat pad weight, found the researchers.

Dr. Yu and colleagues reported that adipogenic genes (LPL, FAT, SREBP-1c and FAS) were markedly up-regulated by rosiglitazone supplementation. Fish oil supplementation increased LPL and FAT, but not SREBP-1c or FAS; however, stained muscle sections indicated no lipid accumulation in skeletal muscle.

Researchers noted that transgenic mice fed a fish oil supplementation had increased expression of adipogenic and glucose uptake genes, leading to reduced plasma glucose concentration.

Natural regulator

The authors suggested that polyunsaturated fatty acids, particularly EPA and DHA, may serve as a natural regulator of glucose uptake in vivo, stating that such effects are mainly mediated through PPARγ activation.

“Our data demonstrated that the PPARγ-regulated glucose metabolism genes, GLUT-4 and ADN were dramatically increased in skeletal muscle of PPARγ transgenic mice when fed rosiglitazone or fish oil, suggesting activation … by either ligand,” concluded the authors.

Source: Journal of Nutritional Biochemistry

“The function of porcine PPARγ and dietary fish oil effect on the expression of lipid and glucose metabolism related genes”

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