scholarly journals Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants?

Diabetologia ◽  
2009 ◽  
Vol 52 (9) ◽  
pp. 1846-1851 ◽  
Author(s):  
L. Southam ◽  
N. Soranzo ◽  
S. B. Montgomery ◽  
T. M. Frayling ◽  
M. I. McCarthy ◽  
...  
PLoS ONE ◽  
2010 ◽  
Vol 5 (11) ◽  
pp. e14040 ◽  
Author(s):  
Christopher G. Bell ◽  
Sarah Finer ◽  
Cecilia M. Lindgren ◽  
Gareth A. Wilson ◽  
Vardhman K. Rakyan ◽  
...  

2014 ◽  
Vol 10 (1) ◽  
pp. 20130853 ◽  
Author(s):  
J. Colette Berbesque ◽  
Frank W. Marlowe ◽  
Peter Shaw ◽  
Peter Thompson

The idea that hunter–gatherer societies experience more frequent famine than societies with other modes of subsistence is pervasive in the literature on human evolution. This idea underpins, for example, the ‘thrifty genotype hypothesis’. This hypothesis proposes that our hunter–gatherer ancestors were adapted to frequent famines, and that these once adaptive ‘thrifty genotypes’ are now responsible for the current obesity epidemic. The suggestion that hunter–gatherers are more prone to famine also underlies the widespread assumption that these societies live in marginal habitats. Despite the ubiquity of references to ‘feast and famine’ in the literature describing our hunter–gatherer ancestors, it has rarely been tested whether hunter–gatherers suffer from more famine than other societies. Here, we analyse famine frequency and severity in a large cross-cultural database, in order to explore relationships between subsistence and famine risk. This is the first study to report that, if we control for habitat quality, hunter–gatherers actually had significantly less—not more—famine than other subsistence modes. This finding challenges some of the assumptions underlying for models of the evolution of the human diet, as well as our understanding of the recent epidemic of obesity and type 2 diabetes mellitus.


2021 ◽  
Vol 22 (9) ◽  
pp. 4495
Author(s):  
Hyunmi Kim ◽  
Da Som Lee ◽  
Tae Hyeon An ◽  
Hyun-Ju Park ◽  
Won Kon Kim ◽  
...  

Liver disease is the spectrum of liver damage ranging from simple steatosis called as nonalcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC). Clinically, NAFLD and type 2 diabetes coexist. Type 2 diabetes contributes to biological processes driving the severity of NAFLD, the primary cause for development of chronic liver diseases. In the last 20 years, the rate of non-viral NAFLD/NASH-derived HCC has been increasing rapidly. As there are currently no suitable drugs for treatment of NAFLD and NASH, a class of thiazolidinediones (TZDs) drugs for the treatment of type 2 diabetes is sometimes used to improve liver failure despite the risk of side effects. Therefore, diagnosis, prevention, and treatment of the development and progression of NAFLD and NASH are important issues. In this review, we will discuss the pathogenesis of NAFLD/NASH and NAFLD/NASH-derived HCC and the current promising pharmacological therapies of NAFLD/NASH. Further, we will provide insights into “adipose-derived adipokines” and “liver-derived hepatokines” as diagnostic and therapeutic targets from NAFLD to HCC.


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