scholarly journals How strongly does appetite counter weight loss? Quantification of the homeostatic control of human energy intake

2016 ◽  
Author(s):  
David Polidori ◽  
Arjun Sanghvi ◽  
Randy Seeley ◽  
Kevin D. Hall

AbstractObjectiveTo quantify the homeostatic feedback control of energy intake in response to long-term covert manipulation of energy balance in free-living humans.MethodsWe used a validated mathematical method to calculate energy intake changes during a 52 week placebo-controlled trial in 153 patients treated with canagliflozin, a sodium glucose co-transporter inhibitor that increases urinary glucose excretion thereby resulting in weight loss without patients being directly aware of the energy deficit. We analyzed the relationship between the body weight time course and the calculated energy intake changes using principles from engineering control theory. ResultsWe discovered that weight loss leads to a proportional homeostatic drive to increase energy intake above baseline by ~100 kcal/day per kg of lost weight – an amount more than 3-fold larger than the corresponding energy expenditure adaptations.ConclusionsWhile energy expenditure adaptations are often thought to be the main reason for slowing of weight loss and subsequent regain, feedback control of energy intake plays an even larger role and helps explain why long-term maintenance of a reduced body weight is so difficult.FundingThis research was supported by the Intramural Research Program of the NIH, National Institute of Diabetes & Digestive & Kidney Diseases, using data from a study sponsored by Janssen Research & Development, LLC.DisclosureD.P. is a full-time employee of Janssen Research & Development, LLC. K.D.H. reports patent pending on a method of personalized dynamic feedback control of body weight (US Patent Application No. 13/754,058; assigned to the NIH) and has received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure. R.S. is a paid consultant for Janssen, Novo Nordisk, Takeda, Daichii Sankyo, Novartis, Pfizer, Nestle, Circuit Therapeutics and Ethicon. R.S., also has received research support from Novo Nordisk, Ethicon, Sanofiand Boehringer Ingelheim. A.S. reports no conflicts of interest.What is already known about this subject?Human body weight is believed to be regulated by homeostatic feedback control of both energy intake and energy expenditure.Adaptations of energy expenditure to weight loss have been well-established, but the homeostatic control of energy intake has yet to be quantified.What this study addsWe provide the first quantification of the homeostatic control of energy intake in free-living humans.The increase in energy intake per kg of weight lost is several-fold larger than the known energy expenditure adaptations.Homeostatic control of energy intake is likely the primary reason why it is difficult to achieve and sustain large weight losses.

1994 ◽  
Vol 72 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Dallas Clark ◽  
Frank Tomas ◽  
Robert T. Withers ◽  
Colin Chandler ◽  
Menno Brinkman ◽  
...  

The doubly-labelled water (2H218O) technique was used to assess the long-term rates of energy expenditure and, after accounting for any changes in body composition, the derived rates of energy intake in weight-stable ‘large-eating’ (n 6) and ‘small-eating’ (n 6) women. The self-reported energy intakes (approximately 11.2 v. 5.6 MJ/d) and energy expenditures (approximately 8.5 v. 12.4 MJ/d) for the ‘large-eating’ and ‘small-eating’ groups respectively, should not be sustainable without significant body-weight changes. 2H218O-assessed rates of energy expenditure for the ‘large-eaters’ (approximately 8.5 MJ/d) and ‘small-eaters’ (approximately 11.3 MJ/d) were in close agreement with the results obtained using 5 d, self-reported activity diaries but the derived rates of energy intake for the ‘large-’ (approximately 8.5 MJ/d) and ‘small-eaters’ (approximately 10.8 MJ/d) were markedly different from those obtained using self-reported, weighed food diaries. When two ‘small-eaters’ were supplied with their self-reported energy intakes (approximately 5 MJ/d) for up to 28 d both subjects lost about 0.75 kg body-weight/week. These results provide no support for the existence of ‘metabolically efficient’ women in the community.


2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.


2004 ◽  
Vol 91 (3) ◽  
pp. 479-484 ◽  
Author(s):  
Alejandro E. Macias

The existence of a set-point for homeostatic control of human body weight is uncertain. To investigate its existence, technically difficult determinations of energy expenditure must be performed: this has resulted in contradictory reports. The present study was performed with new methods in two stages (77 and 133d respectively). Two healthy male subjects with rigorously controlled physical activity ingested three standardized diets of processed foods from the same manufacturer. Hypo-, iso- and hyperenergetic diets containing 6255kJ (1494kcal), 10073kJ (2406kcal) and 13791kJ (3294kcal) respectively were ingested during alternate periods; changes in body weight were measured. A new index of energy expenditure was calculated as the amount of weight lost in an 8h overnight period (WL8H). A digital scale was used in stage 1 and a mechanical scale in stage 2. The change in body weight in response to the isoenergetic diet differed according to the circumstances. In basal conditions, it was associated with weight stability. After weight loss from energy restriction, the isoenergetic diet led to weight gain. After weight gain from overeating, it led to weight loss. Diets of higher energy content were associated with greater WL8H (F>20; P<0·0001 for both subjects). Measurement variability was lower using a mechanical scale. The present study demonstrates the existence of a homeostatic control of human weight and describes a new index of energy expenditure measured in weight units. It also demonstrates that strict dietary supervision for months is possible. Investigation of the human body weight set-point is vital in understanding obesity.


Obesity ◽  
2016 ◽  
Vol 24 (11) ◽  
pp. 2289-2295 ◽  
Author(s):  
David Polidori ◽  
Arjun Sanghvi ◽  
Randy J. Seeley ◽  
Kevin D. Hall

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2533 ◽  
Author(s):  
Christopher L. Melby ◽  
Hunter L. Paris ◽  
R. Drew Sayer ◽  
Christopher Bell ◽  
James O. Hill

Long-term maintenance of weight loss requires sustained energy balance at the reduced body weight. This could be attained by coupling low total daily energy intake (TDEI) with low total daily energy expenditure (TDEE; low energy flux), or by pairing high TDEI with high TDEE (high energy flux). Within an environment characterized by high energy dense food and a lack of need for movement, it may be particularly difficult for weight-reduced individuals to maintain energy balance in a low flux state. Most of these individuals will increase body mass due to an inability to sustain the necessary level of food restriction. This increase in TDEI may lead to the re-establishment of high energy flux at or near the original body weight. We propose that following weight loss, increasing physical activity can effectively re-establish a state of high energy flux without significant weight regain. Although the effect of extremely high levels of physical activity on TDEE may be constrained by compensatory reductions in non-activity energy expenditure, moderate increases following weight loss may elevate energy flux and encourage physiological adaptations favorable to weight loss maintenance, including better appetite regulation. It may be time to recognize that few individuals are able to re-establish energy balance at a lower body weight without permanent increases in physical activity. Accordingly, there is an urgent need for more research to better understand the role of energy flux in long-term weight maintenance.


2012 ◽  
Vol 124 (4) ◽  
pp. 231-241 ◽  
Author(s):  
Priya Sumithran ◽  
Joseph Proietto

Although weight loss can usually be achieved by restricting food intake, the majority of dieters regain weight over the long-term. In the hypothalamus, hormonal signals from the gastrointestinal tract, adipose tissue and other peripheral sites are integrated to influence appetite and energy expenditure. Diet-induced weight loss is accompanied by several physiological changes which encourage weight regain, including alterations in energy expenditure, substrate metabolism and hormone pathways involved in appetite regulation, many of which persist beyond the initial weight loss period. Safe effective long-term strategies to overcome these physiological changes are needed to help facilitate maintenance of weight loss. The present review, which focuses on data from human studies, begins with an outline of body weight regulation to provide the context for the subsequent discussion of short- and long-term physiological changes which accompany diet-induced weight loss.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Ken Kurisu ◽  
Yukari Yamanaka ◽  
Tadahiro Yamazaki ◽  
Ryo Yoneda ◽  
Makoto Otani ◽  
...  

Abstract Background Superior mesenteric artery (SMA) syndrome is a well-known but relatively rare complication of anorexia nervosa. Although several reports have proposed surgery for SMA syndrome associated with anorexia nervosa, these have shown poor outcomes or did not reveal the long-term weight course. Thus, the long-term effectiveness of surgery for SMA syndrome in such cases remains unclear. This case report describes a patient with anorexia nervosa who underwent surgery for SMA syndrome. Case presentation An 18-year-old woman presented with anorexia nervosa when she was 16 years old. She also presented with SMA syndrome, which seemed to be caused by weight loss due to the eating disorder. Nutrition therapy initially improved her body weight, but she ceased treatment. She reported that symptoms related to SMA syndrome had led to her weight loss and desired to undergo surgery. Laparoscopic duodenojejunostomy was performed, but her body weight did not improve after the surgery. The patient eventually received conservative nutritional treatment along with psychological approaches, which led to an improvement in her body weight. Conclusions The case implies that surgery for SMA syndrome in patients with anorexia nervosa is ineffective for long-term weight recovery and that conservative treatment can sufficiently improve body weight; this is consistent with the lack of evidence on the topic and reports on potential complications of surgery. Due to difficulties in assessing psychological status, consultation with specialists on eating disorders is necessary for treating patients with severely low body weight.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joanna Moro ◽  
Catherine Chaumontet ◽  
Patrick C. Even ◽  
Anne Blais ◽  
Julien Piedcoq ◽  
...  

AbstractTo study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and to assess the role of FGF21 in the adaptation to a low protein diet. Thirty-six weanling rats were fed diets containing 3%, 5%, 8%, 12%, 15% and 20% protein for three weeks. Body weight, food intake, energy expenditure and metabolic parameters were followed throughout this period. The very low-protein diets (3% and 5%) induced a large decrease in body weight gain and an increase in energy intake relative to body mass. No gain in fat mass was observed because energy expenditure increased in proportion to energy intake. As expected, Fgf21 expression in the liver and plasma FGF21 increased with low-protein diets, but Fgf21 expression in the hypothalamus decreased. Under low protein diets (3% and 5%), the increase in liver Fgf21 and the decrease of Fgf21 in the hypothalamus induced an increase in energy expenditure and the decrease in the satiety signal responsible for hyperphagia. Our results highlight that when dietary protein decreases below 8%, the liver detects the low protein diet and responds by activating synthesis and secretion of FGF21 in order to activate an endocrine signal that induces metabolic adaptation. The hypothalamus, in comparison, responds to protein deficiency when dietary protein decreases below 5%.


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