Moderate Weight Loss and Sulfonylurea Treatment of Non—insulin-dependent Diabetes Mellitus

Liu, George C.; Coulston, Ann M.; Lardinois, Claude K.; Hollenbeck, C. B.; Moore, Jorene; Reaven, Gerald M.

doi:10.1001/archinte.1985.00360040087020

Cited by 44 publications

(14 citation statements)

References 13 publications

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“…The effect of circulating insulin concentrations or insulin therapy may vary according to the clinical circumstances. The results presented in Table 7 are typical, although some studies report little if any effect on HDL cholesterol (90). In contrast, alleviation of insulin resistance could lessen insulin-stimulated hepatic overproduction of VLDL, particularly in obese diabetic subjects.…”

Section: Indirect Control Of Diabetic Dyslipidemia Through Glycemic Mmentioning

confidence: 75%

“…The latter mechanism, however, has been called into question by in vitro studies that suggest that insulin has an inhibitory effect on VLDL secretion in isolated hepatocytes (84,85). It is well established that weight reduction can produce favorable changes in diabetic dyslipidemia (89)(90)(91)(92). For example, suppression of free fatty acid flux by insulin therapy could lessen the overproduction of VLDL in poorly controlled diabetic subjects.…”

Section: Indirect Control Of Diabetic Dyslipidemia Through Glycemic Mmentioning

confidence: 99%

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Dyslipidemia in type II Diabetes: Implications for Therapeutic Intervention

Stern

Haffner

1991

Diabetes Care

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Cardiovascular disease, and in particular ischemic heart disease, is the principal cause of morbidity, functional disability, and mortality in patients with non-insulin-dependent (type II) diabetes. The main risk factors for the macrovascular complications of diabetes are dyslipidemia, hypertension, and cigarette smoking. Although degree of hyperglycemia is a risk factor for microvascular complications, it is not a prominent risk factor for macrovascular complications. Nevertheless, there are theoretical reasons for believing that glycemic control could lower cardiovascular risk. For example, glycemic control may both improve clearance and suppress hepatic overproduction of very-low-density lipoprotein. Moreover, there is direct empirical evidence that improved glycemic control can favorably alter lipid profiles in type II diabetic patients. Despite this, the only clinical trial that has assessed cardiovascular mortality as an end point in diabetic subjects (i.e., the University Group Diabetes Program) failed to demonstrate a benefit of glycemic control. In this study, the insulin-variable group, which achieved sustained glycemic control relative to the placebo group, had essentially the same cardiovascular mortality as the latter group. All of the conventional lipid-lowering agents have been shown to produce favorable changes in lipid profiles in diabetic subjects. However, the optimum regimen remains to be defined. Metabolic differences between diabetic and nondiabetic subjects mean that the optimum lipid-lowering regimens for the two categories of patients may differ. For example, nicotinic acid, which is a powerful lipid-altering drug, may worsen glucose intolerance. The characteristic lipid abnormalities in type II diabetic subjects are hypertriglyceridemia and low high-density lipoprotein cholesterol, not hypercholesterolemia. Although the role of hypertriglyceridemia as a cardiovascular risk factor in the general population has been questioned, there is evidence that this lipid abnormality may play a stronger role in diabetic subjects. For all of the above reasons, there is an urgent need for large-scale clinical trials assessing cardiovascular end points and testing various strategies of improving lipid profiles in diabetic subjects, particularly given the fact that all of the current generation of lipid-lowering trials have systematically excluded diabetic patients.

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Section: Indirect Control Of Diabetic Dyslipidemia Through Glycemic Mmentioning

confidence: 75%

Section: Indirect Control Of Diabetic Dyslipidemia Through Glycemic Mmentioning

confidence: 99%

Dyslipidemia in type II Diabetes: Implications for Therapeutic Intervention

Stern

Haffner

1991

Diabetes Care

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“…There is recent evidence that, if introduced during the early phase of NIDDM, addition of sulfonylurea treatment to dietary regulation may keep blood glucose levels near normal for at least 2-3 yr (33). Moreover, sulfonylurea "secondary failures" often turn out to be dietary rather than true drug failures, and reintroduction of proper dietary restriction may restore the efficacy of sulfonylureas (34).…”

Section: Why Sulfonylureas?mentioning

confidence: 99%

Sulfonylureas Why, Which, and How?

1990

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Although controversies remain as to the usefulness of sulfonylureas, most evidence is in favor of their use in many if not patients with non-insulin-dependent diabetes mellitus. When used properly, sulfonylureas improve insulin secretion and action, and these effects may be maintained for years. If combined with hypocaloric dietary regulation, rapid- and short-acting sulfonylureas may help patients reach and maintain euglycemia without provoking chronic hyperinsulinemia or weight increase. There is no evidence that sulfonylurea treatment causes beta-cell exhaustion; instead, the antihyperglycemic effect helps improve beta-cell function. Sulfonylurea "failures" are often dietary failures or may be due to late introduction of these drugs, i.e., when beta-cell function is already attenuated. Desensitization of the insulinotropic effect of sulfonylureas may occur but might be avoided by discontinuous (less than 24 h/day) sulfonylurea exposure, i.e., once-daily administration of a short-acting sulfonylurea in a moderate dose. The most important adverse effect of sulfonylureas is long-lasting hypoglycemia, which may lead to permanent neurological damage and even death. This is mainly seen in elderly subjects who are exposed to some intercurrent event, e.g., acute energy deprivation or a drug interaction, i.e., aspirin. Long-acting sulfonylureas may be more likely to promote long-lasting hypoglycemia. The dose-response relationships of sulfonylureas have been poorly investigated, and sulfonylurea therapy should always be initiated and maintained at the lowest possible dose.

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“…Obesity also exacerbates many chronic conditions (e.g., hypertension, dyslipidemia) (4,17,34,43,52). Weight loss has been associated with improvement in risk factors associated with CHD (i.e., blood pressure, serum cholesterol, triglycerides) (6), hypertension (24,36), insulin sensitivity, and other risk factors associated with diabetes mellitus (hepatic glucose production, insulin secretion (22,32). More than one third of U.S. adults are overweight and the prevalence of overweight has increased during the past two decades (25).…”

Section: Introductionmentioning

confidence: 99%

Current Estimates of the Economic Cost of Obesity in the United States

1998

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WOLF, ANNE M., GRAHAM A. COLDITZ. Current estimates of the economic cost of obesity in the United States. Obes Res. 1998;6:97-106 This study was undertaken to update and revise the estimate of the economic impact of obesity in the United States. A prevalence-based approach to the cost of illness was used to estimate the economic costs in 1995 dollars attributable to obesity for type 2 diabetes mellitus, coronary heart disease (CHD), hypertension, gallbladder disease, breast, endometrial and colon cancer, and osteoarthritis. Additionally and independently, excess physician visits, work-lost days, restricted activity, and bed-days attributable to obesity were analyzed cross-sectionally using the 1988 and 1994 National Health Interview Survey (NHIS). Direct (personal health care, hospital care, physician services, allied health services, and medications) and indirect costs (lost output as a result of a reduction or cessation of productivity due to morbidity or mortality) are from published reports and inflated to 1995 dollars using the medical component of the consumer price index (CPI) for direct cost and the all-items CPI for indirect cost. data, cost of lost productivity attributed to obesity (BMI230) was $3.9 billion and reflected 39.2 million days of lost work. In addition, 239 million restrictedactivity days, 89.5 million bed-days, and 62.6 million physician visits were attributable to obesity in 1994. Compared with 1988 NHIS data, in 1994 the number of restricted-activity days (36%), bed-days (28%), and work-lost days (50%) increased substantially. The number of physician visits attributed to obesity increased 88% from 1988 to 1994. The economic and personal health costs of overweight and obesity are enormous and compromise the health of the United States. The direct costs associated with obesity represent 5.7% of our National Health Expenditure in the United States.

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Moderate Weight Loss and Sulfonylurea Treatment of Non—insulin-dependent Diabetes Mellitus

Cited by 44 publications

References 13 publications

Dyslipidemia in type II Diabetes: Implications for Therapeutic Intervention

Dyslipidemia in type II Diabetes: Implications for Therapeutic Intervention

Sulfonylureas Why, Which, and How?

Current Estimates of the Economic Cost of Obesity in the United States

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