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Physiology and Biochemistry

Energy-balance and carbohydrate-insulin models of obesity are not competing propositions

International Journal of Obesity volume 47, pages 95–97 (2023)Cite this article

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The word obese in Latin is meant to convey ‘having eaten until fat’ and the word adipose in Latin means ‘consisting of fat’ [1, 2]. Both these words illustrate the association of obesity with increased accumulation of body fat. Excess calories consumed are deposited in the form of excess body fat in and around viscera leading to obesity and associated comorbidities. Energy-balance model of obesity posits that ‘unconscious awareness’ mediated by endocrine, neural, and hormonal signals act on brain leading to excessive food intake [3]. Carbohydrate-insulin model of obesity emphasizes the role of increased intake of processed carbohydrates acting directly on brain stimulating food intake and producing hyperinsulinemia leading to obesity [4]. The authors of the two models concur in the proposition that a simple “calories in and calories out” cannot be an explanation of obesity (as evidenced by the titles of their recent articles) [3, 5]. The proponents of both models have improved upon their previous versions by incorporating the role of brain as the main organ responding to and controlling food intake [3, 4].

Risk factors for obesity would include genetic, hormonal, environmental, and nutritional factors as widely reviewed in the literature. As I have noted before, the two models could be operative in different sets of individuals [6]. One line of evidence in support of this concept is that diet can induce either inflammatory or insulinemic response in the causation of obesity and type 2 diabetes [7]. Obesity causation explained by energy-balance model would be applicable to individuals with inflammatory responses to diet while in others obesity causation can be explained by carbohydrate-insulin model that is related to insulinemic responses to diet. Several animal studies (mainly in mice) show that high-fat-diet induced obesity is frequently observed in those that have their immune responses biased to Th1 type or proinflammatory responses. This is in line with inflammatory and energy-balance ideas whereas evidence from human studies as cited above can identify causation of obesity to be related to insulinemic response to diet as well [7, 8].

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  1. Department of Biochemistry, Christian Medical College Vellore, Vellore, 632002, India

    Prakash SS

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PSS wrote and revised the manuscript.

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SS, P. Energy-balance and carbohydrate-insulin models of obesity are not competing propositions. Int J Obes 47, 95–97 (2023). https://doi.org/10.1038/s41366-022-01249-2

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