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Discussion Starter · #1 ·
Hi, after waking of a night with hot tingling in my toes and fingers i decided to monitor my fasting blood sugars, after getting readings between 7 and 9.1 i decided to go to GP and request a blood test. I am puzzled as it came back with a 5.2 reading.

I am still getting readings before breakfast at 8 and 9 and still feeling numbness tingling in my feet, but only of a night.

Should i take notice of the labs blood test and just assume all is ok , i am hoping it is but why am i still getting high readings and the burning and tingling???

5,911 Posts
You could request an oral glucose tolerance test. It might show what fastings do not.

Another thing you could do before the GP even gives you any medication for this, is to cut back on carbohydrate consumption, and exercise more and see if those things help.

4,368 Posts
Was that 5.2 a fasting blood test or an HbA1c test. Many times the fasting bg is the last to go. Try doing some bgs test 1 and 2 hours after you eat. If you test much above 120 (6.6) that may indicate diabetes. I would discuss the tingling in your hands and feet it could be caused by many things besides diabetes.
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5 Posts
Discussion Starter · #5 ·
I am in my 60's but am rather active so i'm sure exercise is fine, also i am carefull with diet.

I really don't know if the 5.2 was a fasting blood test or an HbA1c test(i don't know what that is)

I guess it was fasting as i had to fast for 12 hours before the test.

I tried talking to the GP but as the test results came back at 5.2 they tend to disregard it as not important and suggested i should stop taking readings, but i am reluctant to when i know they are up around 8 and 9 at times.

The readings 2 hours after meals are usually between 7 and 8

I think i will go back again and discuss it further.

3,076 Posts
There are hormones which normally come about late in the night before you wake up. These hormones signal the liver to release glucose from its stores to prepare you for the day ahead. In a functioning system, as soon as this glucose begins to appear, the pancreas puts out insulin. This insulin signals the liver to STOP secreting the glucose into the blood and so the whole process only results in a modest and appropriate rise in blood sugar just before you wake up.

The problem can be when the liver still "listens" to those first hormones but loses its ability to respond to the insulin signalling which follows it. This is called hepatic insulin resistance. It is one of the features of type 2 diabetes and is very commonly found.

With the huge increase in diabetes in the last 40 years, we should always look for suspects which are new in that period.

secular trends in fructose intake
the predominant carbohydrate responsible for the rise in
caloric consumption associated with the typical western
diet is the monosaccharide fructose, which is consumed
either as sucrose (50% fructose) or as high*fructose corn
syrup (42% or 55% fructose). Before 1900, us americans
consumed approximately 15 g of fructose per day (4%
of total calories), mainly through fruits and vegetables.
Before world war ii, fructose intake had increased to
24 g per day (5% of total calories); by 1977, it was 37 g
per day (7% of total calories); and by 1994, 55 g per day
(10% of total calories). adolescents today consume over
72.8 g per day (12.1% of total calories) of fructose;
20% of teenagers consume 25% or more of their total
calories as fructose.
thus, fructose consumption has
increased fivefold over the last century and more than
doubled in the last 30 years. Food disappearance data
from the economic research service (ers) of the us
Department of agriculture support this secular trend.
although the ers documents partially decreased sucrose
intake per capita, the total annual consumption of caloric
sweeteners per capita has increased from 33 kg to 43 kg
in 30 years.
although the presence of high*fructose
corn syrup in soft drinks has received most of the atten*
high fruit juice intake has also been associated
with childhood obesity.
Currently, americans consume
sugar at a rate of 66.8 kg per year (180 g per day), half of
which is fructose.
Fructose and the metabolic syndrome
many investigators have implicated fructose in the
pathogenesis of the metabolic syndrome
the liver is the principal site of fructose
metabolism, as it possesses the fructose*specific Glut5
although adipocytes possess Glut*5
mrna and protein, the level of this transporter in adipose
tissue is quite low.
the kidney and small intestine also
possess Glut*5 transporters, but their function is to
transport fructose molecules across their lumena, either
for urinary excretion (to eliminate any systemic fructose
that escapes hepatic clearance) or for release into the
portal circulation, which passes directly to the liver. the
hepatic metabolism of fructose is very different to that
of glucose in that it is insulin independent, bypasses the
process of glycolysis, and increases de novo lipogenesis
to a greater extent. indeed, the hepatic metabolism of
fructose is more reminiscent of that of ethanol.
to ethanol, fructose can induce each of the phenomena
associated with the metabolic syndrome (Figure 2).
Fructose is phosphorylated by fructokinase, which uses
atP as the phosphate donor, depleting the hepatocyte of
intracellular atP. the scavenger enzyme amP deami*
nase 1 reclaims additional phosphates from aDP, and
in the process generates the waste product uric acid.
uric acid acts within vascular smooth muscle to inhibit
endothelial nitric oxide synthase and resultant nitric
oxide production, which promotes hypertension.
our group has shown that sugar*sweetened beverage
consumption positively correlates with uric acid and
blood pressure levels in children,
while others have
documented this association in adults.
the uric acid inhibitor allopurinol can reduce blood
pressure in adolescents
and adults with obesity.
hepatic steatosis
owing to the excess substrate load, excess mitochondrial
acetyl*Coa is formed, exceeding the ability of the tri*
carboxylic acid (tCa) cycle to metabolize it. the excess
acetyl*Coa is converted to citrate, exits into the cytosol via
the citrate shuttle, and serves as the substrate for de novo
lipogenesis. acetyl*Coa dimerizes and is decarboxy*
lated to form malonyl*Coa, which inhibits mitochon*
drial β*oxidation. triglycerides newly formed by de novo
can overwhelm the lipid export machin*
ery and precipitate in the liver, forming intrahepatic
lipid and leading to hepatic steatosis.
hepatic insulin resistance
Fructose*1*phosphate activates dual*specificity mitogen*
activated protein kinase kinase 7 (mKK7),
stimulates the hepatic enzyme mitogen*activated protein
kinase 8 (maPK8).
this kinase is thought to be the
bridge between hepatic metabolism and inflamma*
Furthermore, the intermediate diacylglycerol,
which accumulates during de novo lipogenesis acti*
vates hepatic protein kinase C ε type (PKCε).
maPK8 and PKCε trigger serine phosphorylation and
subsequent inactivation of irs*1, which leads to hepatic
insulin resistance.
Dyslipidemia and muscle insulin resistance
Free fatty acids are also formed, which, when packaged as
triglycerides into heavily fat*laden vlDls, are cleared with
low efficiency, causing dyslipidemia and augmenting the
risk of cardiovascular disease.
excess circulating lipid
is also taken up by skeletal muscle to form intramyocellular
lipid, which leads to muscle insulin resistance.
hyperglycemia and t2DM
Fructose, a gluconeogenic precursor, increases synthe*
sis of the forkhead box protein o1 (FoXo1).
insulin resistance, made worse by elevated fructose
concentrations, prevents the phosphorylation of FoXo1,
which allows this protein to enter the nucleus and induce
the transcription of enzymes that promote gluconeo*
genesis. increased hepatic glucose output foments hyper*
glycemia, and is likely to contribute to the development
of t2Dm.
(from: Article)

As you can see, fructose is implicated in just about every aspect of Type 2 diabetes, not to mention many others "diseases of civilization".

You should take steps to eliminate as much fructose as you possibly can from your diet.
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