Endocrine and Metabolic Effects of Experimental Obesity in Man

Sims, Ethan A. H.; Danforth, Elliot; Horton, Edward S.; Bray, George A.; Glennon, Joseph A.; Salans, Lester B.

doi:10.1016/b978-0-12-571129-6.50016-6

Cited by 289 publications

(215 citation statements)

References 40 publications

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“…15,16 One of the mechanisms involved in the development of liver steatosis is the lower insulin sensitivity frequently observed in overweight patients. 17,18 Diabetes mellitus also contributes to the enhanced rate of lipolysis in the adipose tissue, a metabolic pathway normally suppressed by insulin. Although some authors have found no association between the degree of obesity and the severity of fatty metamorphosis, 4 the prevalence and severity of fatty changes in other series, 19±21 as in ours, were positively associated with BMI.…”

Section: Discussionmentioning

confidence: 99%

Liver abnormalities in severely obese subjects: Effect of drastic weight loss after gastroplasty

et al. 1998

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OBJECTIVE: To examine the factors associated with liver steatosis in severely obese subjects and to test the potential reversibility of fatty liver after weight loss. DESIGN: Retrospective clinical study. SUBJECT: 528 obese patients before bariatric surgery and 69 obese subjects of the initial cohort evaluated before and 27 AE 15 months after gastroplasty. MEASUREMENTS: Fatty deposition (scored as mild, moderate or severe) and in¯ammatory changes were evaluated in liver biopsies; clinical (body mass index (BMI), age, gender, duration of obesity) and biological (glucose, triglycerides, liver enzymes) parameters were related to histological ®ndings. RESULTS: 74% of the 528 biopsies showed fatty change, estimated as mild in 41% of cases, moderate in 32% and severe in 27%. The prevalence of steatosis was signi®cantly higher in men than in women (91% vs 70%, P 0.001) and in patients with impaired glucose tolerance or type 2 diabetes compared with nondiabetics (89% vs 69% P 0.001). The severity of the steatosis was associated with BMI (P 0.002) but not with the duration of obesity or the age of the patient. When compared with patients without fatty change, those with liver steatosis had signi®cantly higher fasting plasma glucose (5.5 mmol/l vs 5.1 mmol/l, P 0.007) and triglycerides (1.8 mmol/l vs 1.3 mmol/l, P 0.002). Mean serum liver enzyme activities (alkaline phosphatase, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl-transpeptidase (gGT) were signi®cantly (P`0.001) increased in patients with fatty change but remained within laboratory reference values. In the 69 patients who have been evaluated after a marked weight reduction (732 AE 19 kg), 45% of the biopsies were considered as normal (vs 13% before, P`0.001) while pure fatty change was still observed in 38% of the patients (vs 83% before, P 0.001). However, the severity of the steatosis was signi®cantly (P`0.001) reduced (mild: 62% vs 21%; moderate: 23% vs 37%; severe: 15% vs 42%). In addition, a signi®cant increase of hepatitis was observed in 26% of the biopsies (vs 14% before, P`0.05). CONCLUSIONS: Liver steatosis in obese subjects is associated with men, diabetic status, BMI, higher fasting glucose and hypertriglyceridaemia. Postgastroplasty weight loss reduces liver steatosis, but seems to increase the incidence of in¯ammatory lobular hepatitis.

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Section: Discussionmentioning

confidence: 99%

Liver abnormalities in severely obese subjects: Effect of drastic weight loss after gastroplasty

et al. 1998

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“…One of the few overfeeding studies often claimed to show increased DIT and resistance to weight gain was that carried out on prisoners in Vermont USA by Sims et al 40 Surprisingly, however, a detailed description of this series of experiments 35 does not include data to allow the cost of weight gain to be calculated, and the evidence for increased DIT relies mainly on showing a much greater energy requirement for weight maintenance in experimentally-obese compared to spontaneously-obese subjects. However, another study was undertaken 36 to allow measurements of energy expenditure to be carried out, and calculation of the cost of weight gain from that experiment gives a value of 32 MJakg (Expt 6, Table 7) that is practically identical to that predicted for a gain comprising 60% fat.…”

Section: Overfeeding Studies By Other Groupsmentioning

confidence: 99%

Gluttony and thermogenesis revisited

1999

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The evolutionary and biological signi®cance of adaptive, homeostatic forms of heat production (thermogenesis) is reviewed. After summarizing the role and selective value of thermogenesis in body temperature regulation (shivering and non-shivering thermogenesis) and the febrile response to infection (fever), the review concentrates on dietinduced thermogenesis (DIT). Animal studies indicate that DIT evolved mainly to deal with nutrient-de®cient or unbalanced diets, and re-analysis of twelve overfeeding studies carried out between 1967 and 1999 suggests the same may be so for humans, particularly when dietary protein concentration is varied. This implies that the role of DIT in the regulation of energy balance is secondary to its function in regulating the metabolic supply of essential nutrients. However, individual differences in DIT are much more marked when high-or low-protein diets are overfed, and this could provide a very sensitive method for discriminating between those who are, in metabolic terms, resistant and those who are susceptible to obesity.

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“…As James (1992) points out, studies that have supported the notion of luxuskonsumption (Widdowson, 1936;Widdowson & McCance, 1936;Miller et at. 1967;Sims, 1968;Sims et al , 1973Edholm et al 1970) have only inferred, not measured, the one unambiguously measurable outcome variable; that is, an increased rate of heat output from the body. However, some studies have demonstrated considerable interindividual variability in the rate of weight gain, under the same conditions of overfeeding.…”

Section: Recent Trends In Energy Balance Researchmentioning

confidence: 99%

Appetite, feeding behaviour and energy balance in human subjects

Rj¹

1998

Proc. Nutr. Soc.

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Since the Second World War there has been a secular trend of increased overweight and obesity in societies where people have ad libitum access to Westem-type diets (Royal College of Physicians, 1983;Gregory et al. 1990;White et al. 1991; Department of Health, 1995). Over this time period the economic costs of obesity and the personal costs of being overweight (in terms of reduced quality of life, increased morbidity and mortality) have been well documented (Seidell, 1995). Throughout this period scientific efforts have intensified in attempting to understand the cause of overweight and obesity and in endeavours to produce effective approaches to sustained body-weight reduction. Ironically, the increased governmental, public health and biomedical research efforts aimed at understanding how to reverse current secular trends in body fatness have been accompanied by an escalation of those very trends. We have now reached the remarkable situation in the UK whereby more that half of the adult population has been categorized as collectively overweight and obese (Department of Health, 1995). By considering research trends in the area of human energy balance (EB) over the last two decades it should become apparent that current research has grown out of and built on the research that went before it. Several of the hypotheses of the 1970s and 1980s have been rejected as inoperable in human subjects in the light of the evidence that was collected to evaluate them. It is worth remembering that disproving an hypothesis does not reduce the contribution it has made to scientific understanding. The very process of disproving the hypothesis actually advances science and leads to new avenues of investigation. It is unfortunate that the meticulous process of hypothesis-testing necessarily proceeds at a somewhat slower rate than the problem that we are trying to address: a large prevalence of excess body weight. However, considerable progress has been made over the last two decades in understanding the major factors most likely to alter EB in man and the types of model which are likely to explain how some people become overweight and obese. These insights have proved invaluable in helping us address current issues pertinent to the control of EB and in targeting key research areas for the future. In order to fully illustrate this point it is worth considering the direction of research into obesity and EB over the last couple of decades.

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Endocrine and Metabolic Effects of Experimental Obesity in Man

Cited by 289 publications

References 40 publications

Liver abnormalities in severely obese subjects: Effect of drastic weight loss after gastroplasty

Liver abnormalities in severely obese subjects: Effect of drastic weight loss after gastroplasty

Gluttony and thermogenesis revisited

Appetite, feeding behaviour and energy balance in human subjects

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