Early and long-term effects of acute caloric deprivation in obese diabetic patients

Bauman, William; Schwartz, Ernest; Rose, Herbert G.; Eisenstein, H.Nina; Johnson, David W.

doi:10.1016/0002-9343(88)90500-1

Cited by 25 publications

(19 citation statements)

References 29 publications

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“…In a previous study by us, we found no relationship between prediet insulin levels and ultimate glycemic response but were able to confirm a modest but significant correlation (r = 0.42) between the duration of diabetes and the glycemic level after 10 days of VLCD therapy (49). Several investigators have also found that prediet body mass index and initial weight are unrelated to glycemic response (49,54,57,66). Even prediet treatment with oral hypoglycemic agents or exogenous insulin therapy has not proved to be a major predictor of a poor glycemic response to hypocaloric diet therapy (49).…”

Section: Effect Of Vlcd On Carbohydrate Metabolismmentioning

confidence: 43%

“…One rationale for admitting such patients is the risk associated with unmasking the rare cases of IDDM after complete insulin withdrawal. Diabetic ketoacidosis is more than a theoretical consideration and has occurred in our clinical experience and that of many others (53,54,60). In addition, it is easier to titrate the insulin dose to the VLCD effect in a monitored setting.…”

Section: Practical Aspects Of Treating Obese Niddm With Vlcd Therapymentioning

confidence: 86%

“…There is no question that end-stage renal disease is a contraindication of VLCD therapy, but it is possible that diabetic patients with compromised renal function may benefit from VLCD treatment. For example, one report included 11 NIDDM patients with renal insufficiency (creatinine >1.5 mg/dl) who were treated with VLCD therapy and derived the commonly observed metabolic benefits from the diet without further compromise of renal function (54). In another report, both subclinical proteinuria and creatinine clearance improved after VLCD therapy in obese NIDDM patients (71).…”

Section: Clinical Use Of Vlcd Therapy In Niddmmentioning

confidence: 99%

“…In addition, protein wasting can theoretically be a problem on a protein-restricted VLCD regimen. One must be cautious with VLCD therapy in patients who appear to be NIDDM but in whom IDDM may be masked, such as mildly obese patients on low doses of insulin (53,54,60). Other unique contraindications to consider are diabetic complications that may be exacerbated by rapid glycemic control.…”

Section: Clinical Use Of Vlcd Therapy In Niddmmentioning

confidence: 99%

“…Continuing oral agents pose the risk of hypoglycemia. Although many clinicians wean patients off oral agents (53,54,58,60), it is simpler to discontinue them on the 1st day of the diet and reinstitute them during or after diet therapy if necessary (19). Long-acting agents such as chlorpropamide require prediet discontinuation.…”

Section: Practical Aspects Of Treating Obese Niddm With Vlcd Therapymentioning

confidence: 99%

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Benefits and Limitations of Very-Low-Calorie Diet Therapy in Obese NIDDM

1991

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Weight reduction is one of the most effective therapies for obese non-insulin-dependent diabetes mellitus (NIDDM), but the success rate with conventional diets has been disappointing. The development of very-low-calorie diets (VLCDs) over the last two decades has provided an alternative approach to the treatment of uncomplicated obesity and is increasingly being used to treat obese NIDDM. This review focuses on the role of VLCDs in the treatment of obese NIDDM, the mechanisms underlying their efficacy, and the controversies surrounding their use. VLCDs provide 400-800 cal/day of high-quality protein and carbohydrate fortified with vitamins, minerals, and trace elements. Weight loss is initially very rapid, followed by steady reduction at a rate of 1-3 kg/wk. Metabolic benefits occur quickly with only modest weight reduction, suggesting that caloric restriction plays a more critical role. Multiple mechanisms account for improved glycemic control, including reduced hepatic glucose output, increased insulin action in the liver and peripheral tissues, and enhanced insulin secretion. VLCDs have the added benefit of rapid improvement in concomitant medical problems, particularly hypertension and hyperlipidemia, that could otherwise accelerate the development of some diabetic complications. Numerous controversies surround VLCD therapy, the most critical of which is its safety. However, recent studies indicate that VLCDs are safe for use by obese NIDDM patients in a medical setting closely supervised by an experienced physician. Contraindications to the diet, side effects, and recommended management are reviewed, as well as the role of adjunctive treatments, including behavioral modification and exercise. We present the perspective that, in most cases, the numerous metabolic benefits derived from VLCD therapy by the obese NIDDM patient outweigh its risks. Furthermore, recent data suggest that VLCD therapy may provide long-term benefits to the obese diabetic patient, despite weight regain.

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Section: Effect Of Vlcd On Carbohydrate Metabolismmentioning

confidence: 43%

Section: Practical Aspects Of Treating Obese Niddm With Vlcd Therapymentioning

confidence: 86%

Section: Clinical Use Of Vlcd Therapy In Niddmmentioning

confidence: 99%

Section: Clinical Use Of Vlcd Therapy In Niddmmentioning

confidence: 99%

Section: Practical Aspects Of Treating Obese Niddm With Vlcd Therapymentioning

confidence: 99%

See 3 more Smart Citations

Benefits and Limitations of Very-Low-Calorie Diet Therapy in Obese NIDDM

1991

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Clinical Manifestations of Systemic Lupus Erythematosus

Ward

Studenski²

1990

Arch Intern Med

144

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Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

Williams

2016

Atherosclerosis

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The growing worldwide prevalence of overnutrition and underexertion threatens the gains that we have made against atherosclerotic cardiovascular disease and other maladies. Chronic overnutrition causes the atherometabolic syndrome, which is a cluster of seemingly unrelated health problems characterized by increased abdominal girth and body-mass index, high fasting and postprandial concentrations of cholesterol- and triglyceride-rich apoB-lipoproteins (C-TRLs), low plasma HDL levels, impaired regulation of plasma glucose concentrations, hypertension, and a significant risk of developing overt type 2 diabetes mellitus (T2DM). In addition, individuals with this syndrome exhibit fatty liver, hypercoagulability, sympathetic overactivity, a gradually rising set-point for body adiposity, a substantially increased risk of atherosclerotic cardiovascular morbidity and mortality, and--crucially--hyperinsulinemia. Many lines of evidence indicate that each component of the atherometabolic syndrome arises, or is worsened by, pathway-selective insulin resistance and responsiveness (SEIRR). Individuals with SEIRR require compensatory hyperinsulinemia to control plasma glucose levels. The result is overdrive of those pathways that remain insulin-responsive, particularly ERK activation and hepatic de-novo lipogenesis (DNL), while carbohydrate regulation deteriorates. The effects are easily summarized: if hyperinsulinemia does something bad in a tissue or organ, that effect remains responsive in the atherometabolic syndrome and T2DM; and if hyperinsulinemia might do something good, that effect becomes resistant. It is a deadly imbalance in insulin action. From the standpoint of human health, it is the worst possible combination of effects. In this review, we discuss the origins of the atherometabolic syndrome in our historically unprecedented environment that only recently has become full of poorly satiating calories and incessant enticements to sit. Data are examined that indicate the magnitude of daily caloric imbalance that causes obesity. We also cover key aspects of healthy, balanced insulin action in liver, endothelium, brain, and elsewhere. Recent insights into the molecular basis and pathophysiologic harm from SEIRR in these organs are discussed. Importantly, a newly discovered oxide transport chain functions as the master regulator of the balance amongst different limbs of the insulin signaling cascade. This oxide transport chain--abbreviated 'NSAPP' after its five major proteins--fails to function properly during chronic overnutrition, resulting in this harmful pattern of SEIRR. We also review the origins of widespread, chronic overnutrition. Despite its apparent complexity, one factor stands out. A sophisticated junk food industry, aided by subsidies from willing governments, has devoted years of careful effort to promote overeating through the creation of a new class of food and drink that is low- or no-cost to the consumer, convenient, savory, calorically dense, yet weakly satiating. It is past time for the rest of us ...

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Early and long-term effects of acute caloric deprivation in obese diabetic patients

Cited by 25 publications

References 29 publications

Benefits and Limitations of Very-Low-Calorie Diet Therapy in Obese NIDDM

Benefits and Limitations of Very-Low-Calorie Diet Therapy in Obese NIDDM

Clinical Manifestations of Systemic Lupus Erythematosus

Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

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