Noradrenaline turnover during under- and over-eating in normal weight subjects

O’Dea, Kerin; Esler, Murray; Leonard, P; Stockigt, Jan R.; Nestel, Paul J.

doi:10.1016/0026-0495(82)90178-0

Cited by 178 publications

(74 citation statements)

References 12 publications

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“…70 Several studies have shown that there are neuroendocrine adaptations to a positive energy balance. Indeed, an increase in plasma free-fatty acids, 73 fat oxidation, 74,75 sympathetic nervous system activity, 76,77 insulinemia at euglycemia 78 and leptinemia 79 are all adaptations that contribute to promote over time the re-equilibration of energy balance in the person who gains weight. Because obesity is the common component of these adaptive mechanisms, an increase in body fat appears as a necessary adaptation to recover body weight stability when one is exposed to a lifestyle favoring a positive energy balance.…”

Section: Short Sleep Duration: Association With Glucose Homeostasismentioning

confidence: 99%

The glucostatic theory of appetite control and the risk of obesity and diabetes

Chaput

Tremblay

2008

Int J Obes

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More than 50 years ago, Jean Mayer proposed that changes in blood glucose concentrations or arteriovenous glucose differences are detected by glucoreceptors that affect energy intake. According to this theory, an increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect. The pioneering work of Mayer has recently received support from our group as low glycemia has been shown to be linked with body weight gain prospectively and has been considered as a strong predictor of the amount of weight regained after weight loss. This state of mild hypoglycemia also predicts the increase in depressive symptoms with weight loss and a greater propensity to glucose intolerance and type 2 diabetes, particularly for individuals having short sleep durations. Furthermore, knowledgebased work has been shown to induce a significant increase in spontaneous energy intake being related to changes in glycemic control. In accordance with the glucostatic theory, this oriented review suggests that factors favoring a trend toward hypoglycemia and/or glucose instability might induce excess energy intake, overweight and impaired glucose tolerance. Data also raise the possibility that fat gain might be protective against mild hypoglycemia by providing compensation to the stimuli promoted by a modern environment. Keywords: body weight; glycemia; glucose homeostasis; glucose intolerance; metabolism; weight gainThe identification of the biochemical basis for hunger and meal initiation, and of the signals controlling these neurobiological processes have been the subject of extensive research and debate for some decades regarding the control of food intake. These studies led to the classical lipostatic, 1 aminostatic, 2 and thermostatic 3 theories of food intake control as well as more recent hypotheses. [4][5][6] However, all of these theoretical ideas were preceded by the notion that glucose uptake and utilization played a central and metabolically privileged role in the control of hunger, satiety and the regulation of body energy balance. Although these notions were first discussed and suggested by Carlson in a classic text published in 1916, 7 they were formalized by Jean Mayer into the classical glucostatic theory in the mid 1950s. 8,9 The glucostatic theory of food intake control postulated that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating. Mayer proposed that decreased glucose utilization or 'metabolic hypoglycemia', the point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering 'metabolizing cells', was the signal for meal initiation. In his 1955 paper, Mayer explicitly argued that the glucostatic theory would account for the short-term control of hunger and food intake, whereas he invoked a lipostatic mechanism...

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Section: Short Sleep Duration: Association With Glucose Homeostasismentioning

confidence: 99%

The glucostatic theory of appetite control and the risk of obesity and diabetes

Chaput

Tremblay

2008

Int J Obes

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“…Since alterations in SNS activity originate within the central nervous system a mechanism that links dietary intake with SNS activity is essential; insulin provides such a link. Although described originally in studies involving laboratory rodents, it is clear that the same dietary changes in SNS activity occur in humans (11,12).…”

Section: Diet and Sympathetic Activitymentioning

confidence: 99%

Obesity and the Insulin Resistance Syndrome

Landsberg

1996

Hypertens Res

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“…For instance, an increase in energy intake elicits an increase in sympathetic activity, in normal body weight subjects. 3,4 This activation leads to enhanced energy expenditure, which compensates the surplus energy intake and, therefore, prevents body weight gain. In obesity-prone subjects, a reduced SNS activity, as evaluated by the microneurography technique (MSNA), could contribute to the development of obesity.…”

Section: Introductionmentioning

confidence: 99%

Relationship between sympathetic reactivity and body weight loss in morbidly obese subjects

et al. 2004

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OBJECTIVE:To investigate the possible role of peripheral sympathetic activity in gastric bypass-induced body weight loss. SUBJECTS AND METHODS:In 42 morbidly obese patients (sex: 36 f/6 m; BMI: 46.070.7 kg/m 2 ) undergoing a gastric bypass, the skin vasoconstrictor reflex in answer to a deep inspiration was measured by laser Doppler fluximetry. The extent of vasoconstriction, measured at the second finger of the left hand, was expressed as percent reduction of the basal blood flux (% vasoconstriction). Insulin sensitivity was assessed before surgery in a subset of patients (n ¼ 11), by the method of euglycemic, hyperinsulinemic clamp. Body weight and composition were evaluated before, and 3, 6 and 12 months after surgery. At the same time points, energy intake (kJ/day) was evaluated by means of both food record diary and alimentary anamnesis. RESULTS: The % vasoconstriction, which was significantly (P ¼ 0.01) greater in normoglycemic subjects than in diabetic ones, was also significantly (P ¼ 0.03) related to the extent of insulin sensitivity measured during the euglycemic clamp. The % vasoconstriction showed a significant (P40.0001), positive correlation with weight reduction obtained between the 6th and 12th months following surgery; as a consequence, % vasoconstriction was significantly (P ¼ 0.0004) related to the overall body weight loss achieved during the year following the operation. These correlations remained significant in multiple regression analysis with adjustment for age, initial body weight, plasma glucose and insulin (P ¼ 0.0007 and 0.006, respectively). The % vasoconstriction was also significantly (P ¼ 0.0006), negatively related to energy intake measured 12 months after surgery. CONCLUSIONS: In conditions of stable body weight, the sympathetic nervous system (SNS) reactivity is influenced by the degree of insulin resistance. A high capacity to activate the SNS, measured before surgery, is associated with both a larger gastric bypass-induced weight loss and a lower energy intake, at the phase of weight stabilization.

show abstract

Noradrenaline turnover during under- and over-eating in normal weight subjects

Cited by 178 publications

References 12 publications

The glucostatic theory of appetite control and the risk of obesity and diabetes

The glucostatic theory of appetite control and the risk of obesity and diabetes

Obesity and the Insulin Resistance Syndrome

Relationship between sympathetic reactivity and body weight loss in morbidly obese subjects

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