Posts Tagged ‘Diabetes’

Nature. 2006 Apr 13 “Reactive oxygen species have a causal role in multiple forms of insulin resistance”

Thursday, May 26th, 2011

Nature. 2006 Apr 13;440(7086):944-8.
Reactive oxygen species have a causal role in multiple forms of insulin resistance.
Houstis N, Rosen ED, Lander ES.
Source

Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA.
Abstract

Insulin resistance is a cardinal feature of type 2 diabetes and is characteristic of a wide range of other clinical and experimental settings. Little is known about why insulin resistance occurs in so many contexts. Do the various insults that trigger insulin resistance act through a common mechanism? Or, as has been suggested, do they use distinct cellular pathways? Here we report a genomic analysis of two cellular models of insulin resistance, one induced by treatment with the cytokine tumour-necrosis factor-alpha and the other with the glucocorticoid dexamethasone. Gene expression analysis suggests that reactive oxygen species (ROS) levels are increased in both models, and we confirmed this through measures of cellular redox state. ROS have previously been proposed to be involved in insulin resistance, although evidence for a causal role has been scant. We tested this hypothesis in cell culture using six treatments designed to alter ROS levels, including two small molecules and four transgenes; all ameliorated insulin resistance to varying degrees. One of these treatments was tested in obese, insulin-resistant mice and was shown to improve insulin sensitivity and glucose homeostasis. Together, our findings suggest that increased ROS levels are an important trigger for insulin resistance in numerous settings.

PMID:
16612386
[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez/16612386?dopt=Abstract&holding=f1000,f1000m,isrctn

Insulin Levels and Life Span Studies

Tuesday, December 14th, 2010

Sci. Aging Knowl. Environ., 4 August 2004
Vol. 2004, Issue 31, p. re5
[DOI: 10.1126/sageke.2004.31.re5]

REVIEWS

Murine Models of Life Span Extension

Jason K. Quarrie, and Karl T. Riabowol

The authors are in the Department of Biochemistry and Molecular Biology at the University of Calgary, Calgary, Alberta, Canada, T2N 4N1. E-mail: karl@ucalgary.ca (K.T.R.)

http://sageke.sciencemag.org/cgi/content/full/2004/31/re5

Key Words: life span extension • mouse models • growth hormone • insulin-like growth factor • oxidative damage • caloric restriction

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Abstract: Mice are excellent experimental models for genetic research and are being used to investigate the genetic component of organismal aging. Several mutant mice are known to possess defects in the growth hormone/insulin-like growth factor 1 (GH/IGF-1) neurohormonal pathway and exhibit dwarfism together with extended life span. Their phenotypes resemble those of mice subjected to caloric restriction. Targeted mutations that affect components of this pathway, including the GH receptor, p66Shc, and the IGF-1 receptor (IGF-1R), also extend life span; mutations that affect IGF-1R or downstream components of the pathway decouple longevity effects from dwarfism. These effects on life span may result from an increased capacity to resist oxidative damage.

Citation: J. K. Quarrie, K. T. Riabowol, Murine Models of Life Span Extension. Sci. Aging Knowl. Environ. 2004 (31), re5 (2004)

source: http://sageke.sciencemag.org/cgi/content/abstract/2004/31/re5

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Glycemic Index, Insulin resistance and IGF-1

Monday, December 13th, 2010

There is a link between hair loss and Insulin resistance, glucose intolerance and IGF-1.

The studies below show that men with vertex balding had increased (higher) levels of circulating Insulin Growth Factor-1 (IGF-1) and decreased (lower) levels of circulating Insulin-Like Growth Factor Binding Protein 3 (IGFBP-3).

J Am Acad Dermatol. 1999 Feb;40(2 Pt 1):200-3. “Hormones and hair patterning in men: a role for insulin-like growth factor 1?”

evaluated the function of “sex steroids”, “sex hormone-binding globulin” (SHBG), and “insulin-like growth factor” (IGF-1) in determining hair-loss patterning in men. This study found that “for each 59 ng/mL increase in IGF-1, the odds of having vertex baldness doubled” and that “Testosterone, SHBG, and IGF-1 may be important in determining hair patterning in men.”

J Am Acad Dermatol. 2000 Jun;42(6):1003-7. “Vertex balding, plasma insulin-like growth factor 1, and insulin-like growth factor binding protein 3″ Found that  “Older men with vertex balding have lower circulating levels of IGFBP-3 and higher levels of IGF-1 when controlling for IGFBP-3 level.”

A link between IGF-1 and glucose intolerance / insulin resistance

Studies suggest that insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homoeostasis. The study below indicates that low IGF-1 levels are associated with the development of insulin resistance and provides “further evidence for the possible protective role of IGF-I against development of glucose intolerance.”

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140+ Reasons Why Sugar Is Ruining Your Health

Sunday, November 28th, 2010

The following list was written by Nancy Appleton, Ph.D. (visit her very informative website www.nancyappleton.com), the author of the book Lick The Sugar Habit.

In addition to throwing off the body’s homeostasis, excess sugar may result in a number of other significant consequences. The following is a listing of some of sugar’s metabolic consequences from a variety of medical journals and other scientific publications.

141 Reasons Sugar Ruins Your Health

(Just Kidding, it’s 143)

By Nancy Appleton PhD & G.N. Jacobs

Excerpted from Suicide by Sugar

Used with permission

1. Sugar can suppress your immune system.

2. Sugar upsets the mineral relationships in the body.

3. Sugar can cause juvenile delinquency in children.

4. Sugar eaten during pregnancy and lactation can influence muscle force production in offspring, which can affect an individual’s ability to exercise.

5. Sugar in soda, when consumed by children, results in the children drinking less milk.

6. Sugar can elevate glucose and insulin responses and return them to fasting levels slower in oral contraceptive users.

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IGF-1 is Linked to Cancers, Heart Disease, Type 2 Diabetes and Osteoporosis

Friday, November 19th, 2010

Insulin-like growth hormone (IGF-1) is believed to be linked to Cancers, Heart Disease, Type 2 Diabetes and Osteoporosis. It could be used to predict the risk of these disease. OR does it?

The link does exist:

decreases serum IGF-1 concentration by ~40%, protects against cancer and slows aging in rodents.

Source: Aging Cell. 2008 Oct;7(5):681-7. – Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans.

Plasma levels of insulin-like growth factor I (IGF-I) have been associated with risk of several cancers.

Source: Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):852-61 – Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations.

Variation in the circulating concentrations of the insulin-like growth factor (IGF) system has been implicated in the etiology of chronic diseases including cancer (prostate, breast, colon, and lung), heart disease, type 2 diabetes, and osteoporosis

..

The results of this study lend additional support to the hypothesis that circulating IGF-I concentrations increase the risk of prostate, bladder, colorectal, and breast cancer

Source: Cancer Epidemiol Biomarkers Prev. 2003 Aug;12(8):739-46. Determinants of circulating insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations in a cohort of Singapore men and women. (more…)

Cent Eur J Public Health. 2006 Jun;14(2):78-81. “Association of insulin resistance linked diseases and hair loss in elderly men. Finnish population-based study”

Tuesday, August 17th, 2010

Note: The below is published here for archival purposes.

Cent Eur J Public Health. 2006 Jun;14(2):78-81.

Association of insulin resistance linked diseases and hair loss in elderly men. Finnish population-based study.

Hirsso P, Laakso M, Matilainen V, Hiltunen L, Rajala U, Jokelainen J, Keinänen-Kiukaanniemi S.

University of Oulu, Department of Public Health Science and General Practice, Finland. paivi.hirsso@oulu.fi

Abstract

Previous investigations have shown an association of androgenetic alopecia (AGA) with insulin resistance related disorders such as ischemic heart disease. An association between AGA and anthropometric abnormalities linked with insulin resistance and heredity in women aged 63 years has also been shown.

We therefore compared 63-year-old men with AGA and ones with normal hair status for insulin resistance linked parameters. A population of 245 men aged 63 years, who were participants in a population-based cross-sectional study in the City of Oulu, underwent a medical check-up including assessment of hair status on the Hamilton-Norwood scale and determination of anthropometric measures, blood pressure, fasting glucose and serum lipids.

Fifty eight per cent of the men reported extensive hair loss (grade III-VII). Hypertension and the use of antihypertensive drugs were common among men with AGA (61% vs. 45% and 50% vs. 26%, respectively). The rates of diabetes and hyperinsulinemia (21% vs. 12% and 61% vs. 49%) were higher among men with AGA compared to those with normal hair status but no difference was seen in other factors.

Our findings show that AGA is common among Finnish men aged 63 years but that it is also associated with insulin linked disturbances, such as hypertension and diabetes. Such men developing AGA might benefit from attention in medical check-up.

PMID: 16830609 [PubMed - indexed for MEDLINE]

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J Mol Med. 2008 Jun;86(6):729-34. “Aldosterone in salt-sensitive hypertension and metabolic syndrome”

Sunday, August 1st, 2010

J Mol Med. 2008 Jun;86(6):729-34. Epub 2008 Apr 25.

Aldosterone in salt-sensitive hypertension and metabolic syndrome.

Fujita T.

Department of Nephrology and Endocrinology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. fujita-dis@h.u-tokyo.ac.jp

Abstract

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome.

Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension.

Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats.

Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress.

In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-alpha, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion.

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