Archive for the ‘Insulin’ Category

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

Sugar is a Poison “The Bitter Truth” by Robert Lustig Lecture

Tuesday, May 24th, 2011


I highly recommend you watch this, it’s a must watch.

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If this video is no longer on youtube email me, I have saved a copy of this for my personal archive.

It’s About Insulin Control

Tuesday, May 24th, 2011

Insulin has been dubbed the “hormone of death” by Life Extension Foundation.

Insulin/IGF signaling itself may mediate communication among various tissues to influence organismal longevity.

Not fat, neither calorie restriction per se, insulin is what matters when it comes to longevity.

Reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling. In the Insulin Levels and Life Span Studies article below, you will see a study titled “Extended Longevity in Mice Lacking the Insulin Receptor in Adipose Tissue”, the genetically altered mice (with fat cells unresponsive to insulin) ate all they wanted (55 percent more food than the control mice) and remained thin, they had 70 percent less body fat than the control group.

The genetically altered mice lived 18 percent longer than the control mice.

I found two main camps, one in favor of fat restriction the other calorie restriction. What is at play in my opinion is insulin. When calorie restriction helps with life extension it is actually the insulin control that is increasing longevity.

Insulin release is stimulated in response to grain, starch and sugar consumption.

I’ve posted various articles here on the harmful effects of sugar you might want to check out.

These are other articles relating to insulin: (more…)

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

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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Insulin Resistance Disorders and Androgenetic Alopecia

Tuesday, November 9th, 2010

 

There is a link between hair loss (balding) and high insulin levels in blood.  Multiple studies have shown that men who experience early balding (i.e under the age of 35) tend to have high blood insulin levels. There is a strong prevalence of insulin resistance with androgenetic alopecia (AGA), and more troublesome, there’s an association of androgenetic alopecia (AGA) with insulin-resistance-related disorders such as ischemic heart disease and serious cardiovascular events.

The above is not only true in men. An association between AGA and anthropometric abnormalities (linked with insulin resistance and heredity) was found in women aged 63 years. Female AGA has usually been linked with hyper-androgenism and hirsutism and, most recently, also with polycystic ovarian syndrome (PCOS). Polycystic ovarian syndrome is quite common among Caucasian women, and its association with insulin resistance is well documented.

Further, epidemiological studies have associated androgenetic alopecia (AGA) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance

The following studies show that AGA and high blood insulin levels are connected. The first dated Sept 2000, then June 2003, June 2006, and Oct 2009.

Lancet. 2000 Sep 30;356(9236):1165-6 “Early androgenetic alopecia as a marker of insulin resistance” Found that men under the age of 35 with an early onset of alopecia aged showed a “strikingly increased risk of hyperinsulinaemia and insulin-resistance-associated disorders” (i.e obesity, hypertension, and dyslipidemia). That early androgenetic alopecia could be a clinical marker of insulin resistance.

J Cardiovasc Risk. 2003 Jun;10(3):227-31. “Hair loss, insulin resistance, and heredity in middle-aged women…” Found that female with some markers of insulin resistance have significantly increased risk for female AGA. Paternal history of alopecia seemed to be more common in female AGA compared to women with normal or minimal loss of hair.

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Glucose Intolerance Article – Archived

Thursday, August 19th, 2010

-::- Note: The below is published here for archival purposes -::-
Thanks to medscape.com for this invaluable article

Glucose Intolerance

Author: Samuel T Olatunbosun, MD, FACP, Chief, Internal Medicine, 56th Medical Group, Luke Air Force Base
Coauthor(s): Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP, Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center

Updated: Jul 16, 2010

Background

Several distinct disorders of glucose tolerance exist. The most widely used classification of diabetes mellitus and allied categories of glucose intolerance is that recommended by the World Health Organization (WHO) in 1985. However, the American Diabetes Association (ADA) has proposed a system based on disease etiology instead of on type of pharmacologic treatment.1

The major categories of the disorders of glycemia or disorders of glucose tolerance are as follows:

  • Type 1 diabetes mellitus
  • Type 2 diabetes mellitus
  • Other specific types of diabetes
  • Gestational diabetes mellitus (GDM)2,3,4
  • Impaired glucose tolerance (IGT)
  • Impaired fasting glucose4

Conditions secondarily associated with glucose intolerance also occur.

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Insulin Resistance Article – Archived

Thursday, August 19th, 2010

-::- Note: The below is published here for archival purposes -::-
Thanks to medscape.com for this invaluable article

Insulin Resistance

Background

Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Insulin resistance has also been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis.

The syndromes of insulin resistance actually make up a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and the metabolic syndrome, as well as an extreme insulin-resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics.

The metabolic syndrome —a state of insulin-resistance that is also known as either syndrome X or the dysmetabolic syndrome—has drawn the greatest attention because of its public health importance.

In an effort to clinically identify patients with insulin resistance, various organizations have developed diagnostic criteria. The most commonly used criteria in the United States are those of the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III).

  • NCEP/ATP III criteria for the diagnosis of the metabolic syndrome include the following (diagnosis is made when 3 or more are present):
    • Waist circumference of more than 102 cm in men or more than 88 cm in women
    • Fasting triglyceride level of 150 mg/dL or higher
    • Blood pressure level of 130/85 mm Hg or higher
    • High-density lipoprotein cholesterol (HDL-C) level of less than 40 mg/dL in men or less than 50 mg/dL in women
    • Fasting glucose level of 110 mg/dL or higher (which has been changed to 100 mg/dL to reflect revised criteria for impaired fasting glucose [IFG])

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The British Journal of Psychiatry (2004) 185: 353-354. “Insulin-like growth factors, insulin resistance and schizophrenia”

Thursday, August 19th, 2010

-::- Note: The below is published here for archival purposes -::-

The British Journal of Psychiatry (2004) 185: 353-354

Correspondence

Insulin-like growth factors, insulin resistance and schizophrenia

D. Gunnell

Department of Social Medicine, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK. E-mail: D.J.Gunnell@bristol.ac.uk

J. M. P. Holly

Division of Surgery, University of Bristol, Bristol Royal Infirmary, Bristol, UK

Abel (Abel, 2004) speculates that imprinting of the gene for insulin-like growth factor-II (IGF-II) as well as other genes may be one pathway through which environmental exposures influence the risk of schizophrenia. We too have hypothesised that factors influencing the growth-hormone–IGF axis may contribute to the well-recognised associations of pre-adult exposures with schizophrenia (Gunnell & Holly, 2004).

We feel that evidence for a direct role of IGF-I is more compelling than that for IGF-II (whose biological functions are poorly understood). Possible pathways for an association with IGF-I lie not only in its role in neurodevelopment but also through its role in neuroprotection following brain damage (e.g. following birth asphyxia, head injury or meningitis) (Gluckman et al, 1998). Insulin-like growth factors exert powerful anti-apoptotic actions and low levels may reduce the survival probability of damaged cells. The influence of IGF-I may extend beyond foetal life as low IGF-I is associated with low birth weight, reduced childhood growth and low body mass index, which are, in turn, associated with the development of psychosis (Wahlbeck et al, 2001; Gunnell et al, 2003). It is therefore possible that low IGF-I levels not only impair neurodevelopment but also render individuals more susceptible to neurodevelopmental insults such as traumatic brain injury and hypoxic brain damage (Gunnell & Holly, 2004).

Several lines of direct and indirect evidence support a possible role of IGF-I in the aetiology of schizophrenia (Gunnell & Holly, 2004). Intriguing indirect evidence for the role of IGF-I, as Abel points out, comes from the observation that low levels protect against a range of different cancers (Renehan et al, 2004) and individuals with psychosis, and their families, appear to be at reduced risk of some malignancies. This may well reflect shared genetic influences on IGF levels influencing susceptibility to both schizophrenia and cancer. Evidence for aetiological associations of IGF-II with cancer risk are less consistent than those for IGF-I. A further indirect line of evidence comes from current concern that insulin resistance may both be more common in people with schizophrenia and be precipitated by antipsychotic medication. Prospective studies indicate that low IGF-I levels are associated with the development of insulin resistance (Sandhu et al, 2002). We speculate that the co-occurrence of insulin resistance and psychosis may in part arise through the shared susceptibility of both these disorders associated with low IGF-I levels.

Evaluation of the possible role of the IGF-system in schizophrenia might not only further our understanding of the aetiology of this disorder but also give insights into its prevention and the reduction of comorbidities such as insulin resistance.

REFERENCES

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