Glucose tolerance and obesity

Stunkard, Albert J.; Blumenthal, Stanley A.

doi:10.1016/0026-0495(72)90083-2

Cited by 7 publications

(2 citation statements)

References 7 publications

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“…At first these studies were almost exclusively psychotherapeutic (11,16,32,43,64,65,97). bles were correlated with the data collected in psychotherapy: glucose tolerance tests (86), pedometer (15,80) and timemotion measurements (9) of physical activity, distorting lens (26) and mirror images (89) of the human body, and so on.…”

Section: Introductionmentioning

confidence: 99%

Presidential Address-1974: From Explanation to Action in Psychosomatic Medicine: The Case of Obesity

Stunkard

1975

Psychosomatic Medicine

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160

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Psychosomatic medicine began as a social movement within medicine, designed to counteract the mechanistic and impersonal features that had accompanied the introduction of science into medical education. In its early days, therapeutic inefficacy led to a concentration upon understanding the origins of disorders in which emotional determinants played a role. To a large exten, psychosomatic medicine is still identified with such understanding. Within recent years, however, the development of increasingly effective therapeutic techniques has changed the emphasis in psychosomatic medicine from understanding to action. These developments are particularly well exemplified by the case of obesity. Social investigations have revealed that the prevalence of obesity within populations is determined to a very high degree by social factors, operating in an unplanned and uncontrolled manner...

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Section: Introductionmentioning

confidence: 99%

Presidential Address-1974: From Explanation to Action in Psychosomatic Medicine: The Case of Obesity

Stunkard

1975

Psychosomatic Medicine

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160

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“…Thus, INTRODUCTION It has been suggested that obesity has an important causal role in the development of hyperglycemia (1), hyperlipemia (2,3), hyperinsulinemia (4), and insulin resistance (5). However, considerable controversy still exists over the role of obesity in causing the above metabolic abnormalities (6)(7)(8)(9)(10), and the mechanisms involved remain quite unclear. Furthermore, although it it commonly accepted that weight loss by obese subjects ameliorates these abnormalities (11)(12) FIGURE 1 Schematic representation of a sequential hypothesis relating insulin resistance to hyperinsulinemia and subsequent hypertriglyceridemia.…”

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confidence: 99%

Effects of Weight Reduction on Obesity STUDIES OF LIPID AND CARBOHYDRATE METABOLISM IN NORMAL AND HYPERLIPOPROTEINEMIC SUBJECTS

Olefsky¹,

Reaven²,

Farquhar³

1974

J. Clin. Invest.

486

110

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A B S T R A C T Considerable controversy exists over the purported role of obesity in causing hyperglycemia, hyperlipemia, hyperinsulinemia, and insulin resistance; and the potential beneficial effects of weight reduction remain incompletely defined. Hypertriglyceridemia is one of the metabolic, abnormalities proposed to accompany obesity, and in order to help explain the mechanisms leading to this abnormality we have proposed the following sequential hypothesis: insulin resistance > hyperinsulinemia > accelerated hepatic triglyceride (TG) production > elevated plasma TG concentrations. To test this hypothesis and to gain insight into both the possible role of obesity in causing the above metabolic abnormalities and the potential benefit of weight reduction we studied the effects of weight loss on various aspects of carbohydrate and lipid metabolism in a group of 36 normal and hyperlipoproteinemic subjects. Only weak to absent correlations (r = 0.03 -0.46) were noted between obesity and the metabolic variables measured. This points out that in our study group obesity cannot be the sole, or even the major, cause of these abnormalities in the first place. Further, we have observed marked decreases after weight reduction in fasting plasma TG (mean value: pre-weight reduction, 319 mg/l00 ml; post-weight reduction, 180 mg/100 ml) and cholesterol (mean values: pre-weight reduction, 282 mg/100 ml; post-weight reduction, 223 after weight reduction were also measured and the overall post-weight reduction decrease in insulin response was 48% while the glucose response was relatively unchanged. In a subgroup of patients we studied both the degree of cellular insulin resistance and the rate of hepatic very low density (VLDL) TG production before and after weight reduction. These subjects demonstrated significant decreases after weight reduction in both degree of insulin resistance (33% decrease) and VLDL-TG production rates (40% decrease). Thus, weight reduction has lowered each of the antecedent variables (insulin resistance, hyperinsulinemia, and VLDL-TG production) that according to the above hypothesis lead to hypertriglyceridemia, and we believe the overall scheme is greatly strengthened. Furthermore, the consistent decreases in plasma TG and cholesterol levels seen in all subjects lead us to conclude that weight reduction is an important therapeutic modality for patients with endogenous hypertriglyceridemia.

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