Insulin resistance and "Syndrome X"
Quote:
>On AMT this morning was a broadcast regarding Insulin resistance and
>"Syndrome X" (a combination of dyslipidemia, low HDL, high triglycerides,
>CVD). I need the name of the show, and the physician that was speaking
>that named the combination of symptoms "Syndrome X".
>Renee Roberts
"Syndrome X" or "insulin resistance syndrome" is defined as:
1 resistance to insulin-mediated glucose uptake
2 glucose intolerance
3 hyperinsulinemia
4 increased very low density triglycerides (VLDL)
5 decreased high-density lipoprotein cholesterol (HDL)
6 hypertension
6a Elevated systolic BP during submaximal exercise
7 increased fat mass
The inherited defect is insulin resistance in skeletal
muscles, the other abnormalities are consequences.
(American J of Obstet Gynecol July 1990 292-5)
A study by teams in Australia and the United States confirms
a genetic defect in certain populations with a high risk of
developing obesity-linked disease such as diabetes. The
research defined the defect in a critical metabolic step in
the body's capacity to metabolise sugar. "However, this
discovery is classed as a major breakthrough in that it has
identified a genetic tendency which causes the disorder."
Professor Paul Zimmet, director of the International
Diabetes Institute (Reuter, July 2 1992)
Some types of Type II diabetes in human were linked to gene
locations in 1992.
implications for hundreds of thousands of Americans was
reported in February, 1993. "This is the first clear
definition of a genetic cause of Type II diabetes," said Dr.
Simon Pilkis, chairman of the Department of Physiology and
Biophysics at the Stony Brook Health Sciences Center in New
York. "Moreover, it may be one of the largest single-gene
disorders described to date." "Tools are now available to
screen for gene mutations, and it is only a matter of time
before other genes implicated in Type II diabetes are
identified," Pilkis said. "We will be able to screen
different diabetic populations or the general population for
these mutations, which will tell us whether someone has a
predisposition to diabetes and what category they fall
into." (UPI 02/28/1993)
high levels of insulin during gestation and infancy. High
insulin levels are sometimes caused by excessive serum
glucose in the mother's {*filter*} and leakage of a insulin-
antibody pairs across the placenta. Obese individuals
almost always exhibit high insulin levels.
forces responsible for producing increased glucose
utilization by white adipose tissue, increased total lipid
synthesis with fat accumulation in adipose tissue and the
liver, together with an insulin-resistant state in the
muscles. (Biochemical Journal 1990 267:99-103)
at the onset of obesity. (Am J Clin Nutr 1993;57:851-6)
reduced glucose clearance is already present. This reduced
clearance is accompanied by compensatory hyperinsulinemia,
suggesting that the primary defect is in peripheral tissue
response to insulin and glucose, not defective pancreatic
beta cells. (Annals of Internal Medicine 1990 113:909-915)
Slow glucose removal rate and hyperinsulinemia precede the
development of Type II diabetes in the offspring of diabetic
parents. (Annals of Internal Medicine 1990:113;909-15)
Insulin-mediated glucose disposal is reduced in otherwise
healthy, lean normotensive subjects. Insulin resistance is
present in these hypertension-prone individuals before the
development of hypertension. (Hypertension 1993:21; 273-9)
development of overt hypertension and gain or redistribution
of body fat. Therefore the concept that insulin sensitivity
is low as a result of altered fat distribution has to be
reconsidered" (Lancet 1993; 341: 327-31)
hyperinsulinemia could be a common link between
cardiological Syndrome X and recently postulated metabolic
Syndrome X with the same characteristic finding - insulin
resistance." (Kendereski et al, U of Beograd, Beograd,
Yugoslavia, Abstracts, IJO 1993)
dysfunctions observed in recent-onset obesity; lipid
oxidation may induce a decrease of glucose oxidation,
insulin resistance, and increased fasting insulin secretion.
(DIABETES 1993:42 1010-16)
with more fast-twitch fibers and fewer slow-twitch fibers.
(DIABETES 1993:42 1073-81)
glucose utilization, lipogenesis and the fat accumulation in
white adipose tissue, while producing an insulin resistant
glucose transport im muscles. (Endocrinology 1990:127;6
3246-8)
A large portion of middle aged and elderly people in Western
countries suffer from a combination of metabolic disorders
and cardiovascular risk factors. This combination includes
hyperinsulinemia (elevated insulin levels), insulin
resistance (reduced sensitivity to insulin), hyperlipidemia
(elevated lipid levels), obesity, and hypertension. This
combination is sometimes termed "Syndrome X" or "insulin
resistance syndrome." Amlyin Pharmaceuticals scientists and
others have observed that most subjects with
hyperinsulinemia also have elevated amylin levels, or
hyperamylinemia. The finding that amylin can stimulate
renin [enzyme associated with hypertension] secretion is
consistent with the idea that amylin may be a missing link
between hypertension and the other metabolic disorders.
(From an Amlyin Pharmaceuticals press release)
Insulin resistance and NIDDM are accompanied by a
progressive deterioration of the microcirculation in many
tissues, including the skeletal muscles that provide most of
the body's insulin mediated glucose disposal. Vascular and
circulatory changes causing a decline in muscle {*filter*} flow
may be the cause of the metabolic disorder. (Diabetologia
1993;36:876-9)
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