willbill <trek@worldwide.net> wrote in
news:g0b6m50n4q@enews2.newsguy.com:
> Màck©® wrote:
>
>> On Sat, 10 May 2008 22:15:58 -0500, willbill wrote:
>
>>> sorry quentin, i've no clue about ACE
>>> and possible reduction of insulin resistance,
>>> since i'm a t1 and don't suffer from
>>> insulin resistance
>
>
>> that doesn't mean other type 1s don't have to deal with
>> insulin resistance.
>
>
> kindly provide an approximate percentage
> of type 1s that do have insulin resistance
>
> and give a cite/site while you're at it
>
> = = = = =
>
> out of curiosity, do *you* have insulin resistance?
>
>
> bill g1 since '57
Attached are a few references in the order encountered in a quick search.
The next to last one suggests insulin resistance (metabolic syndrome)
occurs in 12-40% of type 1 diabetics, but it is a second tier journal at
best. The last one which concludes, "The greatest effect of
rosiglitazone occurred in subjects with more pronounced markers of
insulin resistance", didn't have enough information, at least in a quick
scan, to calculate a percentage.
Diabetes Metab Res Rev. 2002 May-Jun;18(3):192-200
Insulin resistance plays a larger role in the type 1 diabetes disease
process than is commonly recognized. The onset of type 1 diabetes is
often heralded by an antecedent illness and/or the onset of puberty, both
conditions associated with insulin resistance. In the face of a damaged
beta-cell and thus reduced insulin secretion, this change is enough to
manifest hyperglycemia. During the first year of clinical disease,
considerable evidence suggests that the occurrence of clinical remission
or 'honeymoon period' is due to a temporary resolution of the insulin-
resistant state present at diagnosis. Intensive diabetes management is
associated with both improved insulin sensitivity and beta-cell function.
This indicates that the historical data on the changes in insulin
secretion post-diagnosis may be inappropriate when designing current
studies. The known physiological relationship between beta-cell function
and insulin sensitivity complicates interpretation of insulin secretion
data obtained as part of prevention or intervention trials. While it is
recommended that at least a subset of subjects participating in these
trials undergo formal measurements of insulin sensitivity to evaluate
effects of therapy on this parameter independent of effects on the beta-
cell, the sample size must be sufficient to determine an effect if
present. Finally, one could speculate that it is possible that subsets of
people with mild manifestations of the type 1 autoimmune disease process
could benefit from treatments aimed at improving the insulin-resistant
state. Copyright 2002 John Wiley & Sons, Ltd.
Diabetes Metab. 2001 Sep;27(4 Pt 2):S19-25.
Puberty is characterised by important physiological and hormonal changes.
In type 1 diabetes, abnormalities in the growth hormone/insulin-like
growth factor-1 (GH/IGF-1) axis play a important role. Spontaneous hyper-
GH secretion arises, with reduced circulating IGF-1 levels, both leading
to a reduction in insulin sensitivity. From a clinical point of view,
these abnormalities are linked to a deterioration glycaemic control,
often more marked in females (in whom the degree of insulin resistance
during puberty seems to be higher). These abnormalities in the GH/IGF-1
axis in may constitute a risk for the development of microangiopathic
complications. Optimisation of insulin therapy has practical limitations
and intensification of insulin therapy poses problems (weight gain,
nocturnal hypoglycaemia). Several alternative therapeutic approaches have
been explored to restore insulin sensitivity, either through a direct
effect on the GH/IGF-1 axis, or through drugs with a direct insulin
sensitivity effect, but all these approaches remain to be confirmed and
the safety and acceptability of these treatments to be established on a
long-term basis.
Diabetes Obes Metab. 2007 Jan;9(1):143-5
AIM: As many overweight people with T1DM are insulin resistant, adjuvant
therapy with insulin sensitising agents, such as
metformin, may be
beneficial. This study evaluated the effect of adjuvant metformin in T1DM
on insulin sensitivity, diabetic control, body composition, quality of
life (QOL) and treatment satisfaction. MATERIALS AND METHODS: A 3-month
prospective open-labelled pilot study of 16 patients aged 18-40 with T1DM
and body mass index (BMI) >25 kg/m(2) was performed. The patients
received 500-850 mg metformin twice daily. Insulin sensitivity, assessed
by a frequently sampled intravenous glucose tolerance test [n=5], body
composition, HbA(1c) and quality of life (QOL) were measured before and
after treatment. A retrospective review of 30 patients with T1DM treated
with metformin for at least 4 months was also performed. BMI, HbA(1c) and
insulin requirements during metformin treatment was compared to pre-
metformin data, and to patients treated with insulin only. RESULTS: In
the pilot study, insulin sensitivity increased significantly from 0.86
+/- 0.33 x 10(-4)/min/(microU/ml) to 1.17 +/- 0.48 x 10(-4)/min/
(microU/ml) after 3 months adjuvant therapy (p = 0.043). This was
associated with a decreased insulin requirement and mean daily blood
glucose. There were no significant changes in HbA(1c) or body
composition. QOL significantly improved (p < 0.002). The retrospective
review revealed an initial reduction in HbA(1c) (0.8 +/- 1.4%, p =
0.001). This effect diminished with prolonged treatment. BMI decreased in
patients remaining on metformin for a 2-year period (0.5 +/- 0.5kg/m(2),
p = 0.042). CONCLUSION: Adjuvant metformin can improve QOL, insulin
sensitivity and glycaemic control in overweight adults with T1DM.
Arq Bras Endocrinol Metabol. 2006 Apr;50(2):250-63. Epub 2006 May 23
Insulin resistance (IR) plays a larger role in the type 1 diabetes
mellitus (T1DM) disease process than commonly recognized. Overweight and
physical inactivity have increased steadily for the last 20-30 years in
children and adolescents in many populations, concurrently with a rising
incidence of T1DM. The role of IR in T1DM has only recently been gaining
acceptance. This review will focus on how IR influences our current
understanding of disease development and metabolic syndrome (MS) in T1DM.
Increases in IR by weight gain and sedentarism, associated to decreased
beta cell mass by autoimmune process, may disrupt normoglycemia in pre-
T1DM individuals. IR may reflect a more aggressive form of autoimmune
disease mediated by immuno-inflammatory factors that also mediate beta
cell destruction (TNF-alpha and IL-6). These concepts are included in the
"accelerator hypothesis". Moreover, family history of T2DM and chronic
hyperglycemia (glucotoxicity), occurring after T1DM diagnosis, contribute
to decrease peripheral glucose uptake. The onset of diabetic nephropathy
(DN) might also contribute to IR and metabolic syndrome (MS) via low-
grade inflammation and increased oxidative stress. MS is found between 12
to 40% in T1DM, especially in patients with advanced DN and poor glycemic
control. These findings have therapeutic and cardiovascular prognostic
implications as children make the transition toward adolescence and young
adulthood T1DM.
Diabetes Care. 2005 Jul;28(7):1562-7.Click here to read
OBJECTIVE: To evaluate the safety and effectiveness of rosiglitazone in
the treatment of overweight subjects with type 1 diabetes. RESEARCH
DESIGN AND METHODS: A total of 50 adult type 1 diabetic subjects with a
baseline BMI > or =27 kg/m(2) were randomly assigned in a double-blind
fashion to take insulin and placebo (n = 25) or insulin and rosiglitazone
4 mg twice daily (n = 25) for a period of 8 months. Insulin regimen and
dosage were modified in all subjects to achieve near-normal glycemic
control. RESULTS: Both groups experienced a significant reduction in HbA
(1c) (A1C) level (rosiglitazone: 7.9 +/- 1.3 to 6.9 +/- 0.7%, P < 0.0001;
placebo: 7.7 +/- 0.8 to 7.0 +/- 0.9%, P = 0.002) and a significant
increase in weight (rosiglitazone: 97.2 +/- 11.8 to 100.6 +/- 16.0 kg, P
= 0.008; placebo: 96.4 +/- 12.2 to 99.1 +/- 15.0, P = 0.016). Baseline
measures of BMI (P = 0.001), total daily insulin dose (P = 0.002), total
cholesterol (P = 0.005), HDL cholesterol (P = 0.001), and LDL cholesterol
(P = 0.02) were predictors of improvement in A1C level only in the group
treated with rosiglitazone. Total daily insulin dose increased in
subjects taking placebo (74.0 +/- 33.8 to 82.0 +/- 48.9 units, P < 0.05
baseline vs. week 32), but it decreased slightly in subjects taking
rosiglitazone (77.5 +/- 28.6 to 75.3 +/- 33.1 units). Both systolic blood
pressure (137.4 +/- 15.6 vs. 128.8 +/- 14.8 mmHg, baseline vs. week 32, P
< 0.02) and diastolic blood pressure (87.2 +/- 9.4 vs. 79.4 +/- 7.2 mmHg,
P < 0.0001) improved in the group treated with rosiglitazone. The total
incidence of hypoglycemia did not differ between groups. CONCLUSIONS:
Rosiglitazone in combination with insulin resulted in improved glycemic
control and blood pressure without an increase in insulin requirements,
compared with insulin- and placebo-treated subjects, whose improved
glycemic control required an 11% increase in insulin dose. Weight gain
and hypoglycemia were similar in both groups at the end of the study. The
greatest effect of rosiglitazone occurred in subjects with more
pronounced markers of insulin resistance.
--
-------
Charly Coughran
ccoughran@DELETE-TO-RESPOND-UCSD.EDU 
Ace inhibitors and insulin resistance 
Linear Mode
