Insulin Sensitivity and Type 2 Diabetes

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Sugars. Insulin has three major effects on glucose metabolism: it decreases hepatic glucose output, it increases glucose utilization in muscle and adipose tissue, and it enhances glycogen production in the liver and muscle. Insulin sensitivity measures the ability to do these effectively. Individuals vary genetically in their insulin sensitivity, some being much more efficient than others (Reaven, 1999). Obesity is related to decreased insulin sensitivity (Kahn et al., 2001), which can also be influenced by fat intake (see Chapter 11) and exercise.

Two prospective cohort studies showed no risk of diabetes from consuming increased amounts of sugars (Colditz et al., 1992; Meyer et al., 2000). Furthermore, a negative association was observed between increased sucrose intake and risk of diabetes (Meyer et al., 2000). Intervention studies that have evaluated the effect of sugar intakes on insulin concentration and insulin resistance portray mixed results. Dunnigan and coworkers (1970) reported no difference in glucose tolerance and plasma insulin concentration after 0 or 31 percent sucrose was consumed for 4 weeks. Reiser and colleagues (1979b) reported that when 30 percent starch was replaced with 30 percent sucrose, insulin concentration was significantly elevated; however, serum glucose concentration did not differ.


TABLE 6-8 Controlled Studies of Low Glycemic Index (GI) Diets on Carbohydrate and Lipid Metabolism in Healthy, Diabetic, and Hyperlipidemic Subjects

Type of Change in Glycated Reference Study Design Diet GI Proteins

Healthy subjects

Jenkins et al., 6 men, 2 wk -41 Fructosamine


Kiens and Richter, 7 young men, 30 d -24 Not reported


Frost et al., 25 women, 3 wk -18 Not reported


Diabetic subjects Collier et al., 1988

7 type I children, 6 wk


Fontvieille et al. 1988

8 type I men and women, 3 wk


Jenkins et al., 1988a

8 type II men and women, 2 wk



Brand et al., 1991

16 type II men and women, 12 wk


Fontvieille et al. 1992

18 type I and II men and women, 5 wk


Wolever et al., 1992a

15 type II men -27

and women, 2 wk


Wolever et al., 6 type II over- -28 Fructosamine

1992b weight men and women, 6 wk


Change in

Glycated Change in Blood

Proteins (%) Lipidsa (%) Commentsb

Not reported Not reported

-32%c,e urinary C-peptide excretion -10%creatinine clearance during the day

Euglycemic hyperinsulinemic clamp showed no difference in glucose uptake between high and low GI diets at low plasma insulin, but glucose uptake was reduced at high plasma insulin with low GI diet

Not reported Not reported

Using short insulin tolerance test, in vivo insulin sensitivity improved after low GI diet


Reduced postprandial glucose response to standard test meal with low GI diet

-8.9% c'd plasma phospholipids -6.1%c'd daily insulin needs

-30%c'd fasting blood glucose

Not significant -11%c,e plasma glucose response to standard meal

-12.1ce -21.1c,e TAG -11%^ fasting blood glucose

-13.3%c,e mean daily blood glucose

-30%c>e urinary C-peptide excretion -29%c,e postbreakfast blood glucose TAG rose on high GI diet (p = 0.027) and fell on low GI diet, but the difference between the two diets was not significant

-22.4%c'e TAG for the 5 subjects with TAG > 2.2 mmol/L



TABLE 6-8 Continued


Study Design

Change in Diet GI

Type of



Frost et al., 1994

25 type II men and women, 12 wk


20 type II men and women, 2 d



Luscombe et al., 1999

21 type II men and women, 4 wk


Hyperlipidemic subjects Jenkins et al., 30 men and

1987b women, 4 wk

Fructosamine a TC = total cholesterol, LDL-C = low density lipoprotein cholesterol, TAG = triacylglycerols, HDL-C = high density lipoprotein cholesterol. b PAI-1 = plasminogen activator inhibitor-1.

GI. There are well-recognized, short-term effects of high versus low GI carbohydrates on several key hormones and metabolites. In particular, compared to regular consumption of low GI carbohydrates, regular consumption of high GI carbohydrates results in high concentrations of circulating glucose and insulin (Table 6-8). In healthy individuals, there also appears to be an amplification of glucose and insulin responses to consumption of high GI foods with repeated consumption (Liljeberg et al., 1999). Based on associations between these metabolic parameters and risk of disease (DeFronzo et al., 1992; Groop and Eriksson, 1992; Haffner et al., 1988b, 1990; Martin et al., 1992; Rossetti et al., 1990; Warram et al., 1990), further controlled studies on GI and risk factors for diabetes are needed. Furthermore, studies are needed on the extent to which consumption of high GI diets might influence the development of diabetes compared to other putative dietary variables that also influence insulin secretion (e.g., dietary fiber).

In prospective epidemiological studies, three of the four published studies support an association between GI and the development of type 2 diabetes (Table 6-9). Data from the Nurses' Health Study illustrated a significant association between the dietary glycemic index and risk of type 2 diabetes that was significant both with and without an adjustment for


Change in


Change in Blood

Proteins (%)

Lipids" (%)



-11.3c d TC

-21.3%c'd fasting blood glucose

-26.3c'd TAG


-5.2c'e TC

-31%c,e 9-h blood glucose profile


-8.3c'e LDL-C

-53% c'd PAI-1 activity

Not significant

+5.7c'e HDL-C

Fasting plasma glucose did not significantly

differ between the diets

Not significant

When TAG > 2

24-h urinary C-peptide was not significantly



-8.8c'e TC

Changes in weight loss and fat intake did

-9.1 c'e LDL-C

not explain the lipid effects

-19.3c'e TAG

c Significant effect (p < 0.05). d Treatment difference (across treatment). e Endpoint difference (between treatment).

c Significant effect (p < 0.05). d Treatment difference (across treatment). e Endpoint difference (between treatment).

cereal fiber intake (Salmerón et al., 1997b). In contrast, the Iowa Women's Health Study showed no significant relationship between GI and the development of type 2 diabetes after adjusting for total dietary fiber, although the association was positive in the GI range of 59 to 71 and then declined with GI values greater than 71 (Meyer et al., 2000). The reasons for the discrepancy between studies are not known, but may be related to the accuracy of dietary intake records, the imprecision in calculating GI from reported diets, and the age of individuals entering the investigations. There are currently no intervention trials in which dietary GI is manipulated and development of chronic diseases monitored; such studies are needed.

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